Epifil: a dynamic model of infection and disease in lymphatic filariasis.
Identifieur interne : 004841 ( PubMed/Checkpoint ); précédent : 004840; suivant : 004842Epifil: a dynamic model of infection and disease in lymphatic filariasis.
Auteurs : M S Chan [Royaume-Uni] ; A. Srividya ; R A Norman ; S P Pani ; K D Ramaiah ; P. Vanamail ; E. Michael ; P K Das ; D A BundySource :
- The American journal of tropical medicine and hygiene [ 0002-9637 ] ; 1998.
Descripteurs français
- KwdFr :
- Adolescent, Adulte, Adulte d'âge moyen, Enfant, Enfant d'âge préscolaire, Facteurs de l'âge, Filariose lymphatique (), Filariose lymphatique (parasitologie), Filariose lymphatique (épidémiologie), Fonctions de vraisemblance, Humains, Hydrocèle (étiologie), Lymphoedème (étiologie), Modèles biologiques, Mâle, Nourrisson, Nouveau-né, Sujet âgé.
- MESH :
- parasitologie : Filariose lymphatique.
- épidémiologie : Filariose lymphatique.
- étiologie : Hydrocèle, Lymphoedème.
- Adolescent, Adulte, Adulte d'âge moyen, Enfant, Enfant d'âge préscolaire, Facteurs de l'âge, Filariose lymphatique, Fonctions de vraisemblance, Humains, Modèles biologiques, Mâle, Nourrisson, Nouveau-né, Sujet âgé.
English descriptors
- KwdEn :
- Adolescent, Adult, Age Factors, Aged, Child, Child, Preschool, Elephantiasis, Filarial (complications), Elephantiasis, Filarial (epidemiology), Elephantiasis, Filarial (parasitology), Humans, Infant, Infant, Newborn, Likelihood Functions, Lymphedema (etiology), Male, Middle Aged, Models, Biological, Testicular Hydrocele (etiology).
- MESH :
- complications : Elephantiasis, Filarial.
- epidemiology : Elephantiasis, Filarial.
- etiology : Lymphedema, Testicular Hydrocele.
- parasitology : Elephantiasis, Filarial.
- Adolescent, Adult, Age Factors, Aged, Child, Child, Preschool, Humans, Infant, Infant, Newborn, Likelihood Functions, Male, Middle Aged, Models, Biological.
Abstract
The lack of a quantitative framework that describes the dynamic relationships between infection and morbidity has constrained efforts aimed at the community-level control of lymphatic filariasis. In this paper, we describe the development and validation of EPIFIL, a dynamic model of filariasis infection intensity and chronic disease. Infection dynamics are modeled using the well established immigration-death formulation, incorporating the acquisition of immunity to infective larvae over time. The dynamics of disease (lymphodema and hydrocele) are modeled as a catalytic function of a variety of factors, including worm load and the impact of immunopathological responses. The model was parameterized using age-stratified data collected from a Bancroftian filariasis endemic area in Pondicherry in southern India. The fitted parameters suggest that a relatively simple model including only acquired immunity to infection and irreversible progression to disease can satisfactorily explain the observed infection and disease patterns. Disease progression is assumed to be a consequence of worm induced damage and to occur at a high rate for hydrocele and a low rate for lymphodema. This suggests that immunopathology involvement may not be a necessary component of observed age-disease profiles. These findings support a central role for worm burden in the initiation and progression of chronic filarial disease.
PubMed: 9790439
Affiliations:
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pubmed:9790439Le document en format XML
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<front><div type="abstract" xml:lang="en">The lack of a quantitative framework that describes the dynamic relationships between infection and morbidity has constrained efforts aimed at the community-level control of lymphatic filariasis. In this paper, we describe the development and validation of EPIFIL, a dynamic model of filariasis infection intensity and chronic disease. Infection dynamics are modeled using the well established immigration-death formulation, incorporating the acquisition of immunity to infective larvae over time. The dynamics of disease (lymphodema and hydrocele) are modeled as a catalytic function of a variety of factors, including worm load and the impact of immunopathological responses. The model was parameterized using age-stratified data collected from a Bancroftian filariasis endemic area in Pondicherry in southern India. The fitted parameters suggest that a relatively simple model including only acquired immunity to infection and irreversible progression to disease can satisfactorily explain the observed infection and disease patterns. Disease progression is assumed to be a consequence of worm induced damage and to occur at a high rate for hydrocele and a low rate for lymphodema. This suggests that immunopathology involvement may not be a necessary component of observed age-disease profiles. These findings support a central role for worm burden in the initiation and progression of chronic filarial disease.</div>
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