LymphedemaV1, PascalFrancis, Corpus, bibRecord, 000A65

EPIFIL : A dynamic model of infection and disease in lymphatic filariasis

Identifieur interne : 000A65 ( PascalFrancis/Corpus ); précédent : 000A64; suivant : 000A66

EPIFIL : A dynamic model of infection and disease in lymphatic filariasis

Auteurs : M. S. Chan ; A. Srividya ; R. A. Norman ; S. P. Pani ; K. D. Ramaiah ; P. Vanamail ; E. Michael ; P. K. Das ; D. A. P. Bundy

Source :

The American journal of tropical medicine and hygiene [ 0002-9637 ] ; 1998.

RBID : Pascal:98-0519331

Descripteurs français

Pascal (Inist)
- Filariose, Système lymphatique, Modèle dynamique, Inde, Wuchereria bancrofti, Brugia malayi.

English descriptors

KwdEn :
- Brugia malayi, Dynamic model, Filariosis, India, Lymphatic system, Wuchereria bancrofti.

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A02	`01`			`@0 AJTHAB`
A03		`1`		`@0 Am. j. trop. med. hyg.`
A05				`@2 59`
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A11	`02`	`1`		`@1 SRIVIDYA (A.)`
A11	`03`	`1`		`@1 NORMAN (R. A.)`
A11	`04`	`1`		`@1 PANI (S. P.)`
A11	`05`	`1`		`@1 RAMAIAH (K. D.)`
A11	`06`	`1`		`@1 VANAMAIL (P.)`
A11	`07`	`1`		`@1 MICHAEL (E.)`
A11	`08`	`1`		`@1 DAS (P. K.)`
A11	`09`	`1`		`@1 BUNDY (D. A. P.)`
A14	`01`			`@1 The Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford @2 Oxford @3 GBR`
A14	`02`			`@1 Vector Control Research Centre, Medical Complex, Indira Nagar @2 Pondicherry @3 IND`
A20				`@1 606-614`
A21				`@1 1998`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 6817 @5 354000070390930220`
A44				`@0 0000 @1 © 1998 INIST-CNRS. All rights reserved.`
A45				`@0 48 ref.`
A47	`01`	`1`		`@0 98-0519331`
A60				`@1 P`
A61				`@0 A`
A64		`1`		`@0 The American journal of tropical medicine and hygiene`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 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.
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C03	`02`	`X`	`FRE`	`@0 Système lymphatique @5 02`
C03	`02`	`X`	`ENG`	`@0 Lymphatic system @5 02`
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C03	`03`	`X`	`ENG`	`@0 Dynamic model @5 04`
C03	`03`	`X`	`SPA`	`@0 Modelo dinámico @5 04`
C03	`04`	`X`	`FRE`	`@0 Inde @2 NG @5 05`
C03	`04`	`X`	`ENG`	`@0 India @2 NG @5 05`
C03	`04`	`X`	`GER`	`@0 Indien @2 NG @5 05`
C03	`04`	`X`	`SPA`	`@0 India @2 NG @5 05`
C03	`05`	`X`	`FRE`	`@0 Wuchereria bancrofti @2 NS @5 06`
C03	`05`	`X`	`ENG`	`@0 Wuchereria bancrofti @2 NS @5 06`
C03	`05`	`X`	`SPA`	`@0 Wuchereria bancrofti @2 NS @5 06`
C03	`06`	`X`	`FRE`	`@0 Brugia malayi @2 NS @5 07`
C03	`06`	`X`	`ENG`	`@0 Brugia malayi @2 NS @5 07`
C03	`06`	`X`	`SPA`	`@0 Brugia malayi @2 NS @5 07`
C07	`01`	`X`	`FRE`	`@0 Nématodose`
C07	`01`	`X`	`ENG`	`@0 Nematode disease`
C07	`01`	`X`	`SPA`	`@0 Nematodosis`
C07	`02`	`X`	`FRE`	`@0 Helminthiase`
C07	`02`	`X`	`ENG`	`@0 Helminthiasis`
C07	`02`	`X`	`SPA`	`@0 Helmintiasis`
C07	`03`	`X`	`FRE`	`@0 Parasitose`
C07	`03`	`X`	`ENG`	`@0 Parasitosis`
C07	`03`	`X`	`SPA`	`@0 Parasitosis`
C07	`04`	`X`	`FRE`	`@0 Infection`
C07	`04`	`X`	`ENG`	`@0 Infection`
C07	`04`	`X`	`SPA`	`@0 Infección`
C07	`05`	`X`	`FRE`	`@0 Asie @2 NG`
C07	`05`	`X`	`ENG`	`@0 Asia @2 NG`
C07	`05`	`X`	`GER`	`@0 Asien @2 NG`
C07	`05`	`X`	`SPA`	`@0 Asia @2 NG`
C07	`06`	`X`	`FRE`	`@0 Nematoda @2 NS`
C07	`06`	`X`	`ENG`	`@0 Nematoda @2 NS`
C07	`06`	`X`	`SPA`	`@0 Nematoda @2 NS`
C07	`07`	`X`	`FRE`	`@0 Nemathelminthia @2 NS`
C07	`07`	`X`	`ENG`	`@0 Nemathelminthia @2 NS`
C07	`07`	`X`	`SPA`	`@0 Nemathelminthia @2 NS`
C07	`08`	`X`	`FRE`	`@0 Helmintha @2 NS`
C07	`08`	`X`	`ENG`	`@0 Helmintha @2 NS`
C07	`08`	`X`	`SPA`	`@0 Helmintha @2 NS`
C07	`09`	`X`	`FRE`	`@0 Invertebrata @2 NS`
C07	`09`	`X`	`ENG`	`@0 Invertebrata @2 NS`
C07	`09`	`X`	`SPA`	`@0 Invertebrata @2 NS`
N21				`@1 341`

Format Inist (serveur)

NO :	PASCAL 98-0519331 INIST
ET :	EPIFIL : A dynamic model of infection and disease in lymphatic filariasis
AU :	CHAN (M. S.); SRIVIDYA (A.); NORMAN (R. A.); PANI (S. P.); RAMAIAH (K. D.); VANAMAIL (P.); MICHAEL (E.); DAS (P. K.); BUNDY (D. A. P.)
AF :	The Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford/Oxford/Royaume-Uni; Vector Control Research Centre, Medical Complex, Indira Nagar/Pondicherry/Inde
DT :	Publication en série; Niveau analytique
SO :	The American journal of tropical medicine and hygiene; ISSN 0002-9637; Coden AJTHAB; Etats-Unis; Da. 1998; Vol. 59; No. 4; Pp. 606-614; Bibl. 48 ref.
LA :	Anglais
EA :	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.
CC :	002B05E03B4D; 235
FD :	Filariose; Système lymphatique; Modèle dynamique; Inde; Wuchereria bancrofti; Brugia malayi
FG :	Nématodose; Helminthiase; Parasitose; Infection; Asie; Nematoda; Nemathelminthia; Helmintha; Invertebrata
ED :	Filariosis; Lymphatic system; Dynamic model; India; Wuchereria bancrofti; Brugia malayi
EG :	Nematode disease; Helminthiasis; Parasitosis; Infection; Asia; Nematoda; Nemathelminthia; Helmintha; Invertebrata
GD :	Indien
SD :	Filariosis; Sistema linfático; Modelo dinámico; India; Wuchereria bancrofti; Brugia malayi
LO :	INIST-6817.354000070390930220
ID :	98-0519331

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Pascal:98-0519331

Le 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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<s5>07</s5>
</fC03>
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<s2>NS</s2>
<s5>07</s5>
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<s2>NS</s2>
<s5>07</s5>
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<fC07 i1="01" i2="X" l="SPA"><s0>Nematodosis</s0>
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<fC07 i1="02" i2="X" l="FRE"><s0>Helminthiase</s0>
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<fC07 i1="03" i2="X" l="FRE"><s0>Parasitose</s0>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Parasitosis</s0>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Parasitosis</s0>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Asie</s0>
<s2>NG</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Asia</s0>
<s2>NG</s2>
</fC07>
<fC07 i1="05" i2="X" l="GER"><s0>Asien</s0>
<s2>NG</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Asia</s0>
<s2>NG</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Nematoda</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Nematoda</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Nematoda</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Nemathelminthia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Nemathelminthia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Nemathelminthia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Helmintha</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Helmintha</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Helmintha</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Invertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Invertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Invertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>341</s1>
</fN21>
</pA>
</standard>
<server><NO>PASCAL 98-0519331 INIST</NO>
<ET>EPIFIL : A dynamic model of infection and disease in lymphatic filariasis</ET>
<AU>CHAN (M. S.); SRIVIDYA (A.); NORMAN (R. A.); PANI (S. P.); RAMAIAH (K. D.); VANAMAIL (P.); MICHAEL (E.); DAS (P. K.); BUNDY (D. A. P.)</AU>
<AF>The Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford/Oxford/Royaume-Uni; Vector Control Research Centre, Medical Complex, Indira Nagar/Pondicherry/Inde</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>The American journal of tropical medicine and hygiene; ISSN 0002-9637; Coden AJTHAB; Etats-Unis; Da. 1998; Vol. 59; No. 4; Pp. 606-614; Bibl. 48 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B05E03B4D; 235</CC>
<FD>Filariose; Système lymphatique; Modèle dynamique; Inde; Wuchereria bancrofti; Brugia malayi</FD>
<FG>Nématodose; Helminthiase; Parasitose; Infection; Asie; Nematoda; Nemathelminthia; Helmintha; Invertebrata</FG>
<ED>Filariosis; Lymphatic system; Dynamic model; India; Wuchereria bancrofti; Brugia malayi</ED>
<EG>Nematode disease; Helminthiasis; Parasitosis; Infection; Asia; Nematoda; Nemathelminthia; Helmintha; Invertebrata</EG>
<GD>Indien</GD>
<SD>Filariosis; Sistema linfático; Modelo dinámico; India; Wuchereria bancrofti; Brugia malayi</SD>
<LO>INIST-6817.354000070390930220</LO>
<ID>98-0519331</ID>
</server>
</inist>
</record>

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EPIFIL : A dynamic model of infection and disease in lymphatic filariasis

EPIFIL : A dynamic model of infection and disease in lymphatic filariasis

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