Epifil: a dynamic model of infection and disease in lymphatic filariasis

MS Chan, AN Srividya, R Norman… - American Journal of …, 1998 - dspace.stir.ac.uk
MS Chan, AN Srividya, R Norman, SP Pani, KD Ramaiah, P Vanamail, E Michael, PK Das…
American Journal of Tropical Medicine and Hygiene, 1998dspace.stir.ac.uk
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 …
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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