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      Improved models for the relationship between age and the probability of trypanosome infection in female tsetse, Glossina pallidipes Austen

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      Bulletin of Entomological Research
      Cambridge University Press (CUP)

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          Abstract

          Between 1990 and 1999, at Rekomitjie Research Station, Zambezi Valley, Zimbabwe, 29,360 female G. pallidipes were dissected to determine their ovarian category and trypanosome infection status. Overall prevalences were 3.45 and 2.66% for T. vivax and T. congolense, respectively, declining during each year as temperatures increased from July – December. Fits to age-prevalence data using Susceptible-Exposed-Infective (SEI) and SI compartmental models were statistically better than those obtained using a published catalytic model, which made the unrealistic assumption that no female tsetse survived more than seven ovulations. The improved models require knowledge of fly mortality, estimated separately from ovarian category distributions. Infection rates were not significantly higher for T. vivax than for T. congolense. For T. congolense in field-sampled female G. pallidipes, we found no statistical support for a model where the force of infection was higher at the first feed than subsequently. The long survival of adult female tsetse, combined with feeding at intervals ≤3 days, ensures that post-teneral feeds, rather than the first feed, play the dominant role in the epidemiology of T. congolense infections in G. pallidipes. This is supported by estimates that only about 3% of wild hosts at Rekomitjie were harbouring sufficient T. congolense to ensure that tsetse feeding off them take an infected meal, so that the probability of ingesting an infected meal is low at every meal.

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          maxLik: A package for maximum likelihood estimation in R

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            Age-Grouping Methods in Diptera of Medical Importance: With Special Reference to Some Vectors of Malaria

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              A general model for the African trypanosomiases.

              A general mathematical model of a vector-borne disease involving two vertebrate host species and one insect vector species is described. The model is easily extended to other situations involving more than two hosts and one vector species. The model, which was developed from the single-host model for malaria described by Aron & May (1982), is applied to the African trypanosomiases and allows for incubation and immune periods in the two host species and for variable efficiency of transmission of different trypanosome species from the vertebrates to the vectors and vice versa. Equations are derived for equilibrium disease prevalence in each of the species involved. Model predictions are examined by 3-dimensional phase-plane analysis, which is presented as a simple extension of the 2-dimensional phase-plane analysis of the malaria model. Parameter values appropriate for the African trypanosomiases are derived from the literature, and a typical West African village situation is considered, with 300 humans, 50 domestic animals and an average population of 5000 tsetse flies. The model predicts equilibrium prevalences of Trypanosoma vivax, T. congolense and T. brucei of 47.0, 45.8 and 28.7% respectively in the animal hosts, 24.2, 3.4 and 0.15% in the tsetse vectors, and a 7.0% infection of humans with human-infective T. brucei. The contribution to the basic rate of reproduction of the human-infective T. brucei is only 0.11 from the human hosts and 2.54 from the animal hosts, indicating that in the situation modelled human sleeping sickness cannot be maintained in the human hosts alone. The animal reservoir is therefore crucial in determining not only the continued occurrence of the disease in humans, but its prevalence in these hosts as well. The effect of changing average fly density on equilibrium disease prevalences is examined, together with the effect of seasonal changes in fly numbers on disease incidence. In a seasonal situation changes in fly mortality rates affect both future population size and infection rate. Peak disease incidence lags behind peak fly numbers, and that in the less favoured host lags behind that in the more favoured host. Near the threshold fly density for disease transmission disease incidence is more changeable than at higher fly densities and may even exceed equilibrium prevalence at the same average fly density (because most hosts are susceptible at the time that fly numbers begin their annual increase).(ABSTRACT TRUNCATED AT 400 WORDS)
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                Author and article information

                Contributors
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                Journal
                Bulletin of Entomological Research
                Bull. Entomol. Res.
                Cambridge University Press (CUP)
                0007-4853
                1475-2670
                August 2023
                May 17 2023
                August 2023
                : 113
                : 4
                : 469-480
                Article
                10.1017/S0007485323000159
                0421b2be-1461-4109-a680-13f9100a9c07
                © 2023

                Free to read

                https://creativecommons.org/licenses/by/4.0/

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