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Joseph B Hinnebusch - One of the best experts on this subject based on the ideXlab platform.

  • correction comparative ability of oropsylla montana and xenopsylla cheopis Fleas to transmit yersinia pestis by two different mechanisms
    PLOS Neglected Tropical Diseases, 2017
    Co-Authors: Joseph B Hinnebusch, Christopher F Bosio, David M Bland, Clayton O. Jarrett
    Abstract:

    Background Transmission of Yersinia pestis by Flea Bite can occur by two mechanisms. After taking a blood meal from a bacteremic mammal, Fleas have the potential to transmit the very next time they feed. This early-phase transmission resembles mechanical transmission in some respects, but the mechanism is unknown. Thereafter, transmission occurs after Yersinia pestis forms a biofilm in the proventricular valve in the Flea foregut. The biofilm can impede and sometimes completely block the ingestion of blood, resulting in regurgitative transmission of bacteria into the Bite site. In this study, we compared the relative efficiency of the two modes of transmission for Xenopsylla cheopis, a Flea known to become completely blocked at a high rate, and Oropsylla montana, a Flea that has been considered to rarely develop proventricular blockage. Methodology/Principal findings Fleas that took an infectious blood meal containing Y. pestis were maintained and monitored for four weeks for infection and proventricular blockage. The number of Y. pestis transmitted by groups of Fleas by the two modes of transmission was also determined. O. montana readily developed complete proventricular blockage, and large numbers of Y. pestis were transmitted by that mechanism both by it and by X. cheopis, a Flea known to block at a high rate. In contrast, few bacteria were transmitted in the early phase by either species. Conclusions A model system incorporating standardized experimental conditions and viability controls was developed to more reliably compare the infection, proventricular blockage and transmission dynamics of different Flea vectors, and was used to resolve a long-standing uncertainty concerning the vector competence of O. montana. Both X. cheopis and O. montana are fully capable of transmitting Y. pestis by the proventricular biofilm-dependent mechanism.

  • Comparative Ability of Oropsylla montana and Xenopsylla cheopis Fleas to Transmit Yersinia pestis by Two Different Mechanisms.
    Public Library of Science (PLoS), 2017
    Co-Authors: Joseph B Hinnebusch, Christopher F Bosio, David M Bland, Clayton O. Jarrett
    Abstract:

    BACKGROUND:Transmission of Yersinia pestis by Flea Bite can occur by two mechanisms. After taking a blood meal from a bacteremic mammal, Fleas have the potential to transmit the very next time they feed. This early-phase transmission resembles mechanical transmission in some respects, but the mechanism is unknown. Thereafter, transmission occurs after Yersinia pestis forms a biofilm in the proventricular valve in the Flea foregut. The biofilm can impede and sometimes completely block the ingestion of blood, resulting in regurgitative transmission of bacteria into the Bite site. In this study, we compared the relative efficiency of the two modes of transmission for Xenopsylla cheopis, a Flea known to become completely blocked at a high rate, and Oropsylla montana, a Flea that has been considered to rarely develop proventricular blockage. METHODOLOGY/PRINCIPAL FINDINGS:Fleas that took an infectious blood meal containing Y. pestis were maintained and monitored for four weeks for infection and proventricular blockage. The number of Y. pestis transmitted by groups of Fleas by the two modes of transmission was also determined. O. montana readily developed complete proventricular blockage, and large numbers of Y. pestis were transmitted by that mechanism both by it and by X. cheopis, a Flea known to block at a high rate. In contrast, few bacteria were transmitted in the early phase by either species. CONCLUSIONS:A model system incorporating standardized experimental conditions and viability controls was developed to more reliably compare the infection, proventricular blockage and transmission dynamics of different Flea vectors, and was used to resolve a long-standing uncertainty concerning the vector competence of O. montana. Both X. cheopis and O. montana are fully capable of transmitting Y. pestis by the proventricular biofilm-dependent mechanism

  • dermal neutrophil macrophage and dendritic cell responses to yersinia pestis transmitted by Fleas
    PLOS Pathogens, 2015
    Co-Authors: Jeffrey G Shannon, Christopher F Bosio, Joseph B Hinnebusch
    Abstract:

    Yersinia pestis, the causative agent of plague, is typically transmitted by the Bite of an infected Flea. Many aspects of mammalian innate immune response early after Y. pestis infection remain poorly understood. A previous study by our lab showed that neutrophils are the most prominent cell type recruited to the injection site after intradermal needle inoculation of Y. pestis, suggesting that neutrophil interactions with Y. pestis may be important in bubonic plague pathogenesis. In the present study, we developed new tools allowing for intravital microscopy of Y. pestis in the dermis of an infected mouse after transmission by its natural route of infection, the Bite of an infected Flea. We found that uninfected Flea Bites typically induced minimal neutrophil recruitment. The magnitude of neutrophil response to Flea-transmitted Y. pestis varied considerably and appeared to correspond to the number of bacteria deposited at the Bite site. Macrophages migrated towards Flea Bite sites and interacted with small numbers of Flea-transmitted bacteria. Consistent with a previous study, we observed minimal interaction between Y. pestis and dendritic cells; however, dendritic cells did consistently migrate towards Flea Bite sites containing Y. pestis. Interestingly, we often recovered viable Y. pestis from the draining lymph node (dLN) 1 h after Flea feeding, indicating that the migration of bacteria from the dermis to the dLN may be more rapid than previously reported. Overall, the innate cellular host responses to Flea-transmitted Y. pestis differed from and were more variable than responses to needle-inoculated bacteria. This work highlights the importance of studying the interactions between Fleas, Y. pestis and the mammalian host to gain a better understanding of the early events in plague pathogenesis.

  • Association of Flea-transmitted Y. pestis with eGFPdim macrophages in the dermis in vivo.
    2015
    Co-Authors: Jeffrey G Shannon, Christopher F Bosio, Joseph B Hinnebusch
    Abstract:

    A Lys-eGFP mouse ear after being fed upon for 50 min by 5 Y. pestis pMcherry blocked Fleas. Confocal images of ~1 h 17 min and 2 h time points (~1.5 h and 2.25 h post feeding, respectively) of a 4 h movie are shown. The full time series can be seen in S7 Video. The Flea Bite site was identified by Sytox Blue staining prior to acquisition of time series. Images were digitally magnified 6X from original. Arrowhead in each panel indicates Y. pestis (red) associated with the same GFPdim macrophage (green) at each time point. Scale bar represents 20 μm.

  • Imaging and tracking dendritic cell movement in response to Flea Bites and Flea-transmitted Y. pestis in vivo.
    2015
    Co-Authors: Jeffrey G Shannon, Christopher F Bosio, Joseph B Hinnebusch
    Abstract:

    CD11c-YFP mouse ears were fed upon by 1 uninfected Flea for 10 min, Y. pestis pMcherry blocked Fleas for 50 min (No Transmission = 5 Fleas, +Transmission = 6 Fleas), or no Fleas (empty feeding chamber) for 10 min and imaged by confocal microscopy for 4 h. (A) Flea Bite sites were identified by Sytox Blue staining (blue, upper panels only). Upper panels show t = 0 h and lower panels show t = 4 h. The full time series can be seen in S9–S12 Videos. Movement of YFP+ over the course of the experiment was tracked using the image-processing software Imaris. The lower panels also show the cell tracking data and displacement (arrows) for all displacement events ≥ 30 μm. YFP+ cells are dendritic cells (yellow), the red channel shows Y. pestis pMcherry, if present. All examples shown are representative of at least 3 independent experiments. Scale bar represents 100 μm. (B) The direction and length of net displacement were calculated and analysis was limited to displacement events ≥ 30 μm. The direction of cell displacement was manually scored as being “toward,” “neutral,” or “away” from the Flea Bite site (determined by the presence of bacteria and/or Sytox Blue staining). For the No Fleas condition, a spot at the center of the image field was arbitrarily chosen as the reference point for the scoring. The results shown are the mean of at 3 or 4 independent experiments. Error bars represent standard deviation. (C), The average numbers of displacement events ≥ 30 μm in length for each experimental condition were calculated. Error bars represent SEM. The results shown are a mean of 3 or 4 independent experiments. * = p≤0.05, ** = p≤0.01, and **** = p≤0.0001.

Elizabeth García - One of the best experts on this subject based on the ideXlab platform.

  • Prevalence of papular urticaria caused by Flea Bites and associated factors in children 1-6 years of age in Bogotá, D.C.
    The World Allergy Organization journal, 2017
    Co-Authors: Evelyne Halpert, Elizabeth Borrero, Milcíades Ibáñez-pinilla, Pablo Chaparro, Jorge Molina, Maritza Torres, Elizabeth García
    Abstract:

    Papular urticaria is a chronic inflammatory disease caused by exposure to arthropod Bites. The disease has been reported in children attending medical centers, but the causes as the risk factors associated with the disease have not been established. The objective of this study was to determine the prevalence of papular urticaria caused by Flea Bite and identify the risk factors in children between 1 to 6 years of age in Bogota D.C, between March 2009 and June 2011. A cross-sectional, two-stage, clustered study using random probability sampling and stratified with proportional allocation was carried out in children (1–6 years of age) in educational institutions in Bogota D.C. to determine the prevalence of the disease. Children underwent a dermatological examination by general practitioners with a previous training. Furthermore, digital photographs of skin lesions were taken for further confirmation of the diagnosis by dermatologists. A structured survey was completed by the parents or caregivers, and it was evaluated using an unconditional logistic regression to identify factors associated with the disease. A total of 2437 children were included in the study. The prevalence of papular urticaria caused by Flea Bite in this population was 20.3% (CI 95%: 18.2 to 22.5%). The major risk factors associated with the disease were the presence of Fleas in households (OR 1.74, CI 95%: 1.35 to 2.25), using mattresses without springs (OR 1.73, CI 95%: 1.20 to 2.50), the use of daily public transportation to carry the children to the educational institutions (OR 1.76, CI 95%: 1.07 to 2.89), having a soil/earth floor in the main bedroom (OR 6.81, CI 95%:1.16–39.96), and having siblings with a history of atopic dermatitis (OR 1.76 CI 95%: 1.07–2.89). A high prevalence of papular urticaria caused by Flea Bite was found in Bogota D.C. The main factors associated with the disease might be modified with the implementation of prevention, control strategies in housing, educational institutions, and public transportation.

  • Prevalence of papular urticaria caused by Flea Bites and associated factors in children 1–6 years of age in Bogotá, D.C.
    World Allergy Organization Journal, 2017
    Co-Authors: Evelyne Halpert, Elizabeth Borrero, Milcíades Ibáñez-pinilla, Pablo Chaparro, Jorge Molina, Maritza Torres, Elizabeth García
    Abstract:

    Background Papular urticaria is a chronic inflammatory disease caused by exposure to arthropod Bites. The disease has been reported in children attending medical centers, but the causes as the risk factors associated with the disease have not been established. The objective of this study was to determine the prevalence of papular urticaria caused by Flea Bite and identify the risk factors in children between 1 to 6 years of age in Bogotá D.C, between March 2009 and June 2011. Methods A cross-sectional, two-stage, clustered study using random probability sampling and stratified with proportional allocation was carried out in children (1–6 years of age) in educational institutions in Bogotá D.C. to determine the prevalence of the disease. Children underwent a dermatological examination by general practitioners with a previous training. Furthermore, digital photographs of skin lesions were taken for further confirmation of the diagnosis by dermatologists. A structured survey was completed by the parents or caregivers, and it was evaluated using an unconditional logistic regression to identify factors associated with the disease. Results A total of 2437 children were included in the study. The prevalence of papular urticaria caused by Flea Bite in this population was 20.3% (CI 95%: 18.2 to 22.5%). The major risk factors associated with the disease were the presence of Fleas in households (OR 1.74, CI 95%: 1.35 to 2.25), using mattresses without springs (OR 1.73, CI 95%: 1.20 to 2.50), the use of daily public transportation to carry the children to the educational institutions (OR 1.76, CI 95%: 1.07 to 2.89), having a soil/earth floor in the main bedroom (OR 6.81, CI 95%:1.16–39.96), and having siblings with a history of atopic dermatitis (OR 1.76 CI 95%: 1.07–2.89). Conclusions A high prevalence of papular urticaria caused by Flea Bite was found in Bogotá D.C. The main factors associated with the disease might be modified with the implementation of prevention, control strategies in housing, educational institutions, and public transportation.

  • Differences in IgE mediated basophil degranulation induced by proteic fractions from whole Flea body extract in patients with papular urticaria by Flea Bite and healthy controls
    World Allergy Organization Journal, 2013
    Co-Authors: Omar Dominguez-amorocho, Adriana Cuéllar, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez
    Abstract:

    Background Papular urticaria by Flea Bite (PUFB) is a chronic inflammatory disease in children. The aim of this study was to assess the functional activity of IgE to protein fractions from Flea body extract, through basophil degranulation in PUFB patients and controls. Methods Basophil degranulation, measured by overexpression of CD63 surface molecules, was evaluated by flow cytometry in samples from patients and controls. Cell stimulation was performed with three fractions with different molecular weight from Flea body extract using a Basotest® modified protocol. Mann–Whitney U -test was used for comparisons. Results Specific IgE from PUFB patients and healthy controls induced basophil degranulation to Flea body extract with no significant differences between them (16.2 ± 3.1% vs 13.6 ± 2.8% p = 0.77). However, when Flea extract was analyzed in fractions with proteins ranging different molecular weights, significant differences were observed on the response from patients compared with controls to

  • Differences in IgE mediated basophil degranulation induced by proteic fractions from whole Flea body extract in patients with papular urticaria by Flea Bite and healthy controls.
    The World Allergy Organization journal, 2013
    Co-Authors: Omar Dominguez-amorocho, Adriana Cuéllar, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez
    Abstract:

    Background Papular urticaria by Flea Bite (PUFB) is a chronic inflammatory disease in children. The aim of this study was to assess the functional activity of IgE to protein fractions from Flea body extract, through basophil degranulation in PUFB patients and controls.

  • Differences in systemic and skin migrating-specific CD4 T cells in papular urticaria by Flea Bite.
    International archives of allergy and immunology, 2012
    Co-Authors: Omar Dominguez-amorocho, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez, John Mario González, María Claudia Ortega, Adriana Cuéllar
    Abstract:

    Background: Papular urticaria by Flea Bite is a chronic allergic condition in which clinical improvement may occur at the age of 7 years, thus representing a natu

Clayton O. Jarrett - One of the best experts on this subject based on the ideXlab platform.

  • Comparison of the transmission efficiency and plague progression dynamics associated with two mechanisms by which Fleas transmit Yersinia pestis.
    PLoS pathogens, 2020
    Co-Authors: Christopher F Bosio, Clayton O. Jarrett, Dana P. Scott, Jonathan Fintzi, B. Joseph Hinnebusch
    Abstract:

    Yersinia pestis can be transmitted by Fleas during the first week after an infectious blood meal, termed early-phase or mass transmission, and again after Y. pestis forms a cohesive biofilm in the Flea foregut that blocks normal blood feeding. We compared the transmission efficiency and the progression of infection after transmission by Oropsylla montana Fleas at both stages. Fleas were allowed to feed on mice three days after an infectious blood meal to evaluate early-phase transmission, or after they had developed complete proventricular blockage. Transmission was variable and rather inefficient by both modes, and the odds of early-phase transmission was positively associated with the number of infected Fleas that fed. Disease progression in individual mice bitten by Fleas infected with a bioluminescent strain of Y. pestis was tracked. An early prominent focus of infection at the intradermal Flea Bite site and dissemination to the draining lymph node(s) soon thereafter were common features, but unlike what has been observed in intradermal injection models, this did not invariably lead to further systemic spread and terminal disease. Several of these mice resolved the infection without progression to terminal sepsis and developed an immune response to Y. pestis, particularly those that received an intermediate number of early-phase Flea Bites. Furthermore, two distinct types of terminal disease were noted: the stereotypical rapid onset terminal disease within four days, or a prolonged onset preceded by an extended, fluctuating infection of the lymph nodes before eventual systemic dissemination. For both modes of transmission, bubonic plague rather than primary septicemic plague was the predominant disease outcome. The results will help to inform mathematical models of Flea-borne plague dynamics used to predict the relative contribution of the two transmission modes to epizootic outbreaks that erupt periodically from the normal enzootic background state.

  • correction comparative ability of oropsylla montana and xenopsylla cheopis Fleas to transmit yersinia pestis by two different mechanisms
    PLOS Neglected Tropical Diseases, 2017
    Co-Authors: Joseph B Hinnebusch, Christopher F Bosio, David M Bland, Clayton O. Jarrett
    Abstract:

    Background Transmission of Yersinia pestis by Flea Bite can occur by two mechanisms. After taking a blood meal from a bacteremic mammal, Fleas have the potential to transmit the very next time they feed. This early-phase transmission resembles mechanical transmission in some respects, but the mechanism is unknown. Thereafter, transmission occurs after Yersinia pestis forms a biofilm in the proventricular valve in the Flea foregut. The biofilm can impede and sometimes completely block the ingestion of blood, resulting in regurgitative transmission of bacteria into the Bite site. In this study, we compared the relative efficiency of the two modes of transmission for Xenopsylla cheopis, a Flea known to become completely blocked at a high rate, and Oropsylla montana, a Flea that has been considered to rarely develop proventricular blockage. Methodology/Principal findings Fleas that took an infectious blood meal containing Y. pestis were maintained and monitored for four weeks for infection and proventricular blockage. The number of Y. pestis transmitted by groups of Fleas by the two modes of transmission was also determined. O. montana readily developed complete proventricular blockage, and large numbers of Y. pestis were transmitted by that mechanism both by it and by X. cheopis, a Flea known to block at a high rate. In contrast, few bacteria were transmitted in the early phase by either species. Conclusions A model system incorporating standardized experimental conditions and viability controls was developed to more reliably compare the infection, proventricular blockage and transmission dynamics of different Flea vectors, and was used to resolve a long-standing uncertainty concerning the vector competence of O. montana. Both X. cheopis and O. montana are fully capable of transmitting Y. pestis by the proventricular biofilm-dependent mechanism.

  • Comparative Ability of Oropsylla montana and Xenopsylla cheopis Fleas to Transmit Yersinia pestis by Two Different Mechanisms.
    Public Library of Science (PLoS), 2017
    Co-Authors: Joseph B Hinnebusch, Christopher F Bosio, David M Bland, Clayton O. Jarrett
    Abstract:

    BACKGROUND:Transmission of Yersinia pestis by Flea Bite can occur by two mechanisms. After taking a blood meal from a bacteremic mammal, Fleas have the potential to transmit the very next time they feed. This early-phase transmission resembles mechanical transmission in some respects, but the mechanism is unknown. Thereafter, transmission occurs after Yersinia pestis forms a biofilm in the proventricular valve in the Flea foregut. The biofilm can impede and sometimes completely block the ingestion of blood, resulting in regurgitative transmission of bacteria into the Bite site. In this study, we compared the relative efficiency of the two modes of transmission for Xenopsylla cheopis, a Flea known to become completely blocked at a high rate, and Oropsylla montana, a Flea that has been considered to rarely develop proventricular blockage. METHODOLOGY/PRINCIPAL FINDINGS:Fleas that took an infectious blood meal containing Y. pestis were maintained and monitored for four weeks for infection and proventricular blockage. The number of Y. pestis transmitted by groups of Fleas by the two modes of transmission was also determined. O. montana readily developed complete proventricular blockage, and large numbers of Y. pestis were transmitted by that mechanism both by it and by X. cheopis, a Flea known to block at a high rate. In contrast, few bacteria were transmitted in the early phase by either species. CONCLUSIONS:A model system incorporating standardized experimental conditions and viability controls was developed to more reliably compare the infection, proventricular blockage and transmission dynamics of different Flea vectors, and was used to resolve a long-standing uncertainty concerning the vector competence of O. montana. Both X. cheopis and O. montana are fully capable of transmitting Y. pestis by the proventricular biofilm-dependent mechanism

  • differential control of yersinia pestis biofilm formation in vitro and in the Flea vector by two c di gmp diguanylate cyclases
    PLOS ONE, 2011
    Co-Authors: Yicheng Sun, Clayton O. Jarrett, Frank C. Gherardini, Alexandra Koumoutsi, Kevin A Lawrence, Creg Darby, Joseph B Hinnebusch
    Abstract:

    Yersinia pestis forms a biofilm in the foregut of its Flea vector that promotes transmission by Flea Bite. As in many bacteria, biofilm formation in Y. pestis is controlled by intracellular levels of the bacterial second messenger c-di-GMP. Two Y. pestis diguanylate cyclase (DGC) enzymes, encoded by hmsT and y3730, and one phosphodiesterase (PDE), encoded by hmsP, have been shown to control biofilm production in vitro via their opposing c-di-GMP synthesis and degradation activities, respectively. In this study, we provide further evidence that hmsT, hmsP, and y3730 are the only three genes involved in c-di-GMP metabolism in Y. pestis and evaluated the two DGCs for their comparative roles in biofilm formation in vitro and in the Flea vector. As with HmsT, the DGC activity of Y3730 depended on a catalytic GGDEF domain, but the relative contribution of the two enzymes to the biofilm phenotype was influenced strongly by the environmental niche. Deletion of y3730 had a very minor effect on in vitro biofilm formation, but resulted in greatly reduced biofilm formation in the Flea. In contrast, the predominant effect of hmsT was on in vitro biofilm formation. DGC activity was also required for the Hms-independent autoaggregation phenotype of Y. pestis, but was not required for virulence in a mouse model of bubonic plague. Our results confirm that only one PDE (HmsP) and two DGCs (HmsT and Y3730) control c-di-GMP levels in Y. pestis, indicate that hmsT and y3730 are regulated post-transcriptionally to differentially control biofilm formation in vitro and in the Flea vector, and identify a second c-di-GMP-regulated phenotype in Y. pestis.

  • transit through the Flea vector induces a pretransmission innate immunity resistance phenotype in yersinia pestis
    PLOS Pathogens, 2010
    Co-Authors: Viveka Vadyvaloo, Florent Sebbane, Clayton O. Jarrett, Daniel E Sturdevant, Joseph B Hinnebusch
    Abstract:

    Yersinia pestis, the agent of plague, is transmitted to mammals by infected Fleas. Y. pestis exhibits a distinct life stage in the Flea, where it grows in the form of a cohesive biofilm that promotes transmission. After transmission, the temperature shift to 37°C induces many known virulence factors of Y. pestis that confer resistance to innate immunity. These factors are not produced in the low-temperature environment of the Flea, however, suggesting that Y. pestis is vulnerable to the initial encounter with innate immune cells at the Flea Bite site. In this study, we used whole-genome microarrays to compare the Y. pestis in vivo transcriptome in infective Fleas to in vitro transcriptomes in temperature-matched biofilm and planktonic cultures, and to the previously characterized in vivo gene expression profile in the rat bubo. In addition to genes involved in metabolic adaptation to the Flea gut and biofilm formation, several genes with known or predicted roles in resistance to innate immunity and pathogenicity in the mammal were upregulated in the Flea. Y. pestis from infected Fleas were more resistant to phagocytosis by macrophages than in vitro-grown bacteria, in part attributable to a cluster of insecticidal-like toxin genes that were highly expressed only in the Flea. Our results suggest that transit through the Flea vector induces a phenotype that enhances survival and dissemination of Y. pestis after transmission to the mammalian host.

Evelyne Halpert - One of the best experts on this subject based on the ideXlab platform.

  • Prevalence of papular urticaria caused by Flea Bites and associated factors in children 1-6 years of age in Bogotá, D.C.
    The World Allergy Organization journal, 2017
    Co-Authors: Evelyne Halpert, Elizabeth Borrero, Milcíades Ibáñez-pinilla, Pablo Chaparro, Jorge Molina, Maritza Torres, Elizabeth García
    Abstract:

    Papular urticaria is a chronic inflammatory disease caused by exposure to arthropod Bites. The disease has been reported in children attending medical centers, but the causes as the risk factors associated with the disease have not been established. The objective of this study was to determine the prevalence of papular urticaria caused by Flea Bite and identify the risk factors in children between 1 to 6 years of age in Bogota D.C, between March 2009 and June 2011. A cross-sectional, two-stage, clustered study using random probability sampling and stratified with proportional allocation was carried out in children (1–6 years of age) in educational institutions in Bogota D.C. to determine the prevalence of the disease. Children underwent a dermatological examination by general practitioners with a previous training. Furthermore, digital photographs of skin lesions were taken for further confirmation of the diagnosis by dermatologists. A structured survey was completed by the parents or caregivers, and it was evaluated using an unconditional logistic regression to identify factors associated with the disease. A total of 2437 children were included in the study. The prevalence of papular urticaria caused by Flea Bite in this population was 20.3% (CI 95%: 18.2 to 22.5%). The major risk factors associated with the disease were the presence of Fleas in households (OR 1.74, CI 95%: 1.35 to 2.25), using mattresses without springs (OR 1.73, CI 95%: 1.20 to 2.50), the use of daily public transportation to carry the children to the educational institutions (OR 1.76, CI 95%: 1.07 to 2.89), having a soil/earth floor in the main bedroom (OR 6.81, CI 95%:1.16–39.96), and having siblings with a history of atopic dermatitis (OR 1.76 CI 95%: 1.07–2.89). A high prevalence of papular urticaria caused by Flea Bite was found in Bogota D.C. The main factors associated with the disease might be modified with the implementation of prevention, control strategies in housing, educational institutions, and public transportation.

  • Prevalence of papular urticaria caused by Flea Bites and associated factors in children 1–6 years of age in Bogotá, D.C.
    World Allergy Organization Journal, 2017
    Co-Authors: Evelyne Halpert, Elizabeth Borrero, Milcíades Ibáñez-pinilla, Pablo Chaparro, Jorge Molina, Maritza Torres, Elizabeth García
    Abstract:

    Background Papular urticaria is a chronic inflammatory disease caused by exposure to arthropod Bites. The disease has been reported in children attending medical centers, but the causes as the risk factors associated with the disease have not been established. The objective of this study was to determine the prevalence of papular urticaria caused by Flea Bite and identify the risk factors in children between 1 to 6 years of age in Bogotá D.C, between March 2009 and June 2011. Methods A cross-sectional, two-stage, clustered study using random probability sampling and stratified with proportional allocation was carried out in children (1–6 years of age) in educational institutions in Bogotá D.C. to determine the prevalence of the disease. Children underwent a dermatological examination by general practitioners with a previous training. Furthermore, digital photographs of skin lesions were taken for further confirmation of the diagnosis by dermatologists. A structured survey was completed by the parents or caregivers, and it was evaluated using an unconditional logistic regression to identify factors associated with the disease. Results A total of 2437 children were included in the study. The prevalence of papular urticaria caused by Flea Bite in this population was 20.3% (CI 95%: 18.2 to 22.5%). The major risk factors associated with the disease were the presence of Fleas in households (OR 1.74, CI 95%: 1.35 to 2.25), using mattresses without springs (OR 1.73, CI 95%: 1.20 to 2.50), the use of daily public transportation to carry the children to the educational institutions (OR 1.76, CI 95%: 1.07 to 2.89), having a soil/earth floor in the main bedroom (OR 6.81, CI 95%:1.16–39.96), and having siblings with a history of atopic dermatitis (OR 1.76 CI 95%: 1.07–2.89). Conclusions A high prevalence of papular urticaria caused by Flea Bite was found in Bogotá D.C. The main factors associated with the disease might be modified with the implementation of prevention, control strategies in housing, educational institutions, and public transportation.

  • Differences in IgE mediated basophil degranulation induced by proteic fractions from whole Flea body extract in patients with papular urticaria by Flea Bite and healthy controls
    World Allergy Organization Journal, 2013
    Co-Authors: Omar Dominguez-amorocho, Adriana Cuéllar, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez
    Abstract:

    Background Papular urticaria by Flea Bite (PUFB) is a chronic inflammatory disease in children. The aim of this study was to assess the functional activity of IgE to protein fractions from Flea body extract, through basophil degranulation in PUFB patients and controls. Methods Basophil degranulation, measured by overexpression of CD63 surface molecules, was evaluated by flow cytometry in samples from patients and controls. Cell stimulation was performed with three fractions with different molecular weight from Flea body extract using a Basotest® modified protocol. Mann–Whitney U -test was used for comparisons. Results Specific IgE from PUFB patients and healthy controls induced basophil degranulation to Flea body extract with no significant differences between them (16.2 ± 3.1% vs 13.6 ± 2.8% p = 0.77). However, when Flea extract was analyzed in fractions with proteins ranging different molecular weights, significant differences were observed on the response from patients compared with controls to

  • Differences in IgE mediated basophil degranulation induced by proteic fractions from whole Flea body extract in patients with papular urticaria by Flea Bite and healthy controls.
    The World Allergy Organization journal, 2013
    Co-Authors: Omar Dominguez-amorocho, Adriana Cuéllar, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez
    Abstract:

    Background Papular urticaria by Flea Bite (PUFB) is a chronic inflammatory disease in children. The aim of this study was to assess the functional activity of IgE to protein fractions from Flea body extract, through basophil degranulation in PUFB patients and controls.

  • Differences in systemic and skin migrating-specific CD4 T cells in papular urticaria by Flea Bite.
    International archives of allergy and immunology, 2012
    Co-Authors: Omar Dominguez-amorocho, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez, John Mario González, María Claudia Ortega, Adriana Cuéllar
    Abstract:

    Background: Papular urticaria by Flea Bite is a chronic allergic condition in which clinical improvement may occur at the age of 7 years, thus representing a natu

Adriana Cuéllar - One of the best experts on this subject based on the ideXlab platform.

  • Differences in IgE mediated basophil degranulation induced by proteic fractions from whole Flea body extract in patients with papular urticaria by Flea Bite and healthy controls
    World Allergy Organization Journal, 2013
    Co-Authors: Omar Dominguez-amorocho, Adriana Cuéllar, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez
    Abstract:

    Background Papular urticaria by Flea Bite (PUFB) is a chronic inflammatory disease in children. The aim of this study was to assess the functional activity of IgE to protein fractions from Flea body extract, through basophil degranulation in PUFB patients and controls. Methods Basophil degranulation, measured by overexpression of CD63 surface molecules, was evaluated by flow cytometry in samples from patients and controls. Cell stimulation was performed with three fractions with different molecular weight from Flea body extract using a Basotest® modified protocol. Mann–Whitney U -test was used for comparisons. Results Specific IgE from PUFB patients and healthy controls induced basophil degranulation to Flea body extract with no significant differences between them (16.2 ± 3.1% vs 13.6 ± 2.8% p = 0.77). However, when Flea extract was analyzed in fractions with proteins ranging different molecular weights, significant differences were observed on the response from patients compared with controls to

  • Differences in IgE mediated basophil degranulation induced by proteic fractions from whole Flea body extract in patients with papular urticaria by Flea Bite and healthy controls.
    The World Allergy Organization journal, 2013
    Co-Authors: Omar Dominguez-amorocho, Adriana Cuéllar, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez
    Abstract:

    Background Papular urticaria by Flea Bite (PUFB) is a chronic inflammatory disease in children. The aim of this study was to assess the functional activity of IgE to protein fractions from Flea body extract, through basophil degranulation in PUFB patients and controls.

  • Differences in systemic and skin migrating-specific CD4 T cells in papular urticaria by Flea Bite.
    International archives of allergy and immunology, 2012
    Co-Authors: Omar Dominguez-amorocho, Evelyne Halpert, Elizabeth García, Silvia Duarte, Adriana Rodríguez, John Mario González, María Claudia Ortega, Adriana Cuéllar
    Abstract:

    Background: Papular urticaria by Flea Bite is a chronic allergic condition in which clinical improvement may occur at the age of 7 years, thus representing a natu

  • Specific pattern of Flea antigen recognition by IgG subclass and IgE during the progression of papular urticaria caused by Flea Bite.
    Allergologia Et Immunopathologia, 2010
    Co-Authors: Adriana Cuéllar, Evelyne Halpert, Alberto Gomez, Adriana Rojas, F. Rojas, A Rodriguez, Elizabeth García
    Abstract:

    BACKGROUND: Papular urticaria caused by Flea Bite presents clinical symptoms of a hypersensitivity reaction accompanied by skin lesions. However, the pattern of recognition by different antibody isotypes during the progression of the disease is unknown. This study evaluated variations in immunoglobulin E and immunoglobulin G subclass antibody responses to Flea antigens during the progression of papular urticaria caused by Flea Bite METHODS: Twenty-five patients clinically diagnosed with papular urticaria due to Flea Bite were included. Ten healthy children were included as controls. Recognition of antigens from complete Flea body extract by patients and healthy controls was determined using immunoblot assays. RESULTS: The results revealed that patients with 2-5 years of papular urticaria evidenced more IgE bands than those with shorter or longer durations of symptoms. In contrast, healthy children showed a predominance of immunoglobulin G1 and immunoglobulin G3. The majority of the recognised antigens were low molecular weight proteins (

  • Specific pattern of Flea antigen recognition by IgG subclass and IgE during the progression of papular urticaria caused by Flea Bite
    Allergologia et immunopathologia, 2010
    Co-Authors: Adriana Cuéllar, Evelyne Halpert, Alberto Gomez, Adriana Rojas, F. Rojas, Adriana Rodríguez, Elizabeth García
    Abstract:

    Abstract Background Papular urticaria caused by Flea Bite presents clinical symptoms of a hypersensitivity reaction accompanied by skin lesions. However, the pattern of recognition by different antibody isotypes during the progression of the disease is unknown. This study evaluated variations in immunoglobulin E and immunoglobulin G subclass antibody responses to Flea antigens during the progression of papular urticaria caused by Flea Bite Methods Twenty-five patients clinically diagnosed with papular urticaria due to Flea Bite were included. Ten healthy children were included as controls. Recognition of antigens from complete Flea body extract by patients and healthy controls was determined using immunoblot assays. Results The results revealed that patients with 2–5 years of papular urticaria evidenced more IgE bands than those with shorter or longer durations of symptoms. In contrast, healthy children showed a predominance of immunoglobulin G1 and immunoglobulin G3. The majority of the recognised antigens were low molecular weight proteins ( Conclusion The predominant specific antibody isotypes vary according to the time elapsed since the onset of symptoms in papular urticaria caused by Flea Bite.