Modelling Lymphatic Filariasis: Transmission and Control

Lymphatic filariasis (LF) is a mosquito borne parasitic disease of the tropics. Of the three species of parasites causing the disease, W. bancrofti transmitted by Culex quinquefasciatus is the most widely prevalent. Infection can lead to disabling chronic manifestations: lymphoedema, elephantiasis, and hydrocele. Transmission can be interrupted either by controlling the vector or parasite. Parasite control through mass drug administration (MDA) of antifilarial drugs seems to be more cost-effective than vector control. MDA can reduce the parasite load in the population, reduce transmission and hence prevent disease. Several countries initiated elimination programmes. Recommending a specific control strategy should be based on prospects of its favourable impact on the epidemiology and disease burden. Mathematical models are invaluable in helping to understand parasite population dynamics, aid decision-making about control strategies and evaluate long-term effects of control measures. This thesis contributed to (i) knowledge and quantification of the population dynamics of W. bancrofti, and (ii) to use this knowledge in the development and application of a simulation model (LYMFASIM). This model is based on the results of an integrated vector management study in Pondicherry, India. Epidemiological analyses indicated that prevalence of microfilaria (mf) in younger population is a better indicator of effectiveness of vector control than overall prevalence or intensity of mf. Assessment based on this indicator demonstrated the superiority of the integrated vector management programme over conventional method of vector control. Both field and experimental transmission studies demonstrated that parasite development in the vector is density-dependent. Simulation model based analysis of longitudinal data indicated that observed epidemiological patterns in Pondicherry are immune mediated. Variations between persons in exposure to vector biting and eliciting immune response are found to be plausible explanations for the observed variability in mf-density in the population. Model predicted trend in prevalence agreed with observations made during pre- and post control periods as well as three and seven years after stopping control. Predictions beyond the period of observations suggested that prevalence would reach the pre-control level 25 years after stopping control. Further application of the model to predict how long MDA to be continued to achieve elimination, showed that six annual MDA with diethylcarbamazine and albendazole would be sufficient if population coverage is 65% per round. The required duration of mass treatment increases with endemicity level.

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