Research article Special Issues

An immuno-epidemiological model linking between-host and within-host dynamics of cholera


  • Received: 10 May 2023 Revised: 24 June 2023 Accepted: 10 July 2023 Published: 04 August 2023
  • Cholera, a severe gastrointestinal infection caused by the bacterium Vibrio cholerae, remains a major threat to public health, with a yearly estimated global burden of 2.9 million cases. Although most existing models for the disease focus on its population dynamics, the disease evolves from within-host processes to the population, making it imperative to link the multiple scales of the disease to gain better perspectives on its spread and control. In this study, we propose an immuno-epidemiological model that links the between-host and within-host dynamics of cholera. The immunological (within-host) model depicts the interaction of the cholera pathogen with the adaptive immune response. We distinguish pathogen dynamics from immune response dynamics by assigning different time scales. Through a time-scale analysis, we characterise a single infected person by their immune response. Contrary to other within-host models, this modelling approach allows for recovery through pathogen clearance after a finite time. Then, we scale up the dynamics of the infected person to construct an epidemic model, where the infected population is structured by individual immunological dynamics. We derive the basic reproduction number ($ \mathcal{R}_0 $) and analyse the stability of the equilibrium points. At the disease-free equilibrium, the disease will either be eradicated if $ \mathcal{R}_0 < 1 $ or otherwise persists. A unique endemic equilibrium exists when $ \mathcal{R}_0 > 1 $ and is locally asymptotically stable without a loss of immunity.

    Citation: Beryl Musundi. An immuno-epidemiological model linking between-host and within-host dynamics of cholera[J]. Mathematical Biosciences and Engineering, 2023, 20(9): 16015-16032. doi: 10.3934/mbe.2023714

    Related Papers:

  • Cholera, a severe gastrointestinal infection caused by the bacterium Vibrio cholerae, remains a major threat to public health, with a yearly estimated global burden of 2.9 million cases. Although most existing models for the disease focus on its population dynamics, the disease evolves from within-host processes to the population, making it imperative to link the multiple scales of the disease to gain better perspectives on its spread and control. In this study, we propose an immuno-epidemiological model that links the between-host and within-host dynamics of cholera. The immunological (within-host) model depicts the interaction of the cholera pathogen with the adaptive immune response. We distinguish pathogen dynamics from immune response dynamics by assigning different time scales. Through a time-scale analysis, we characterise a single infected person by their immune response. Contrary to other within-host models, this modelling approach allows for recovery through pathogen clearance after a finite time. Then, we scale up the dynamics of the infected person to construct an epidemic model, where the infected population is structured by individual immunological dynamics. We derive the basic reproduction number ($ \mathcal{R}_0 $) and analyse the stability of the equilibrium points. At the disease-free equilibrium, the disease will either be eradicated if $ \mathcal{R}_0 < 1 $ or otherwise persists. A unique endemic equilibrium exists when $ \mathcal{R}_0 > 1 $ and is locally asymptotically stable without a loss of immunity.



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    [1] W. Garira, A complete categorization of multiscale models of infectious disease systems, J. Biol. Dyn., 11 (2017), 378–435. https://doi.org/10.1080/17513758.2017.1367849 doi: 10.1080/17513758.2017.1367849
    [2] H. W. Hethcote, Mathematics of infectious diseases, SIAM Rev., 42 (2000), 599–653. https://doi.org/10.1137/S0036144500371907 doi: 10.1137/S0036144500371907
    [3] Z. Feng, J. Velasco-Hernandez, B. Tapia-Santos, M. C. Leite, A model for coupling within-host and between-host dynamics in an infectious disease, Nonlinear Dyn., 68 (2012), 401–411. https://doi.org/10.1007/s11071-011-0291-0 doi: 10.1007/s11071-011-0291-0
    [4] Z. Feng, J. Velasco-Hernandez, B. Tapia-Santos, A mathematical model for coupling within-host and between-host dynamics in an environmentally-driven infectious disease, Math. Biosci., 241 (2013), 49–55. https://doi.org/10.1016/j.mbs.2012.09.004 doi: 10.1016/j.mbs.2012.09.004
    [5] Z. Shuai, P. van den Driessche, Global dynamics of cholera models with differential infectivity, Math. Biosci., 234 (2011), 118–126. https://doi.org/10.1016/j.mbs.2011.09.003 doi: 10.1016/j.mbs.2011.09.003
    [6] X. Wang, J. Wang, Modeling the within-host dynamics of cholera: bacterial–viral interaction, J. Biol. Dyn., 11 (2017), 484–501. https://doi.org/10.1080/17513758.2016.1269957 doi: 10.1080/17513758.2016.1269957
    [7] M. Martcheva, N. Tuncer, C. St Mary, Coupling within-host and between-host infectious diseases models, Biomath, 4 (2015), 1510091. https://doi.org/10.11145/j.biomath.2015.10.091 doi: 10.11145/j.biomath.2015.10.091
    [8] L. M. Childs, F. El Moustaid, Z. Gajewski, S. Kadelka, R. Nikin-Beers, J. W. Smith, et al., Linked within-host and between-host models and data for infectious diseases: a systematic review, PeerJ, 7 (2019), e7057. https://doi.org/10.7717/peerj.7057 doi: 10.7717/peerj.7057
    [9] W. Garira, D. Mathebula, R. Netshikweta, A mathematical modelling framework for linked within-host and between-host dynamics for infections with free-living pathogens in the environment, Math. Biosci., 256 (2014), 58–78. https://doi.org/10.1016/j.mbs.2014.08.004 doi: 10.1016/j.mbs.2014.08.004
    [10] M. Ali, A. R. Nelson, A. L. Lopez, D. A. Sack, Updated global burden of cholera in endemic countries, PLoS Negl. Trop. Dis., 9 (2015), e0003832. https://doi.org/10.1371/journal.pntd.0003832 doi: 10.1371/journal.pntd.0003832
    [11] D. M. Hartley, J. G. Morris, D. L. Smith, Hyperinfectivity: a critical element in the ability of V. cholerae to cause epidemics, PLoS Med., 3 (2006), e7. https://doi.org/10.1371/journal.pmed.0030007 doi: 10.1371/journal.pmed.0030007
    [12] J. Reidl, K. E. Klose, Vibrio cholerae and cholera: out of the water and into the host, FEMS Microbiol. Rev., 26 (2002), 125–139. https://doi.org/10.1016/S0168-6445(02)00091-8 doi: 10.1016/S0168-6445(02)00091-8
    [13] Z. Mukandavire, S. Liao, J. Wang, H. Gaff, D. L. Smith, J. G. Morris, Estimating the reproductive numbers for the 2008-2009 cholera outbreaks in Zimbabwe, PNAS, 108 (2011), 8767–8772. https://doi.org/10.1073/pnas.1019712108 doi: 10.1073/pnas.1019712108
    [14] J. P. Tian, J. Wang, Global stability for cholera epidemic models, Math. Biosci., 232 (2011), 31–41. https://doi.org/10.1016/j.mbs.2011.04.001 doi: 10.1016/j.mbs.2011.04.001
    [15] F. Brauer, Z. Shuai, P. van den Driessche, Dynamics of an age-of-infection cholera model, Math. Biosci. Eng., 10 (2013), 1335–1349. https://doi.org/10.3934/mbe.2013.10.1335 doi: 10.3934/mbe.2013.10.1335
    [16] X. Wang, J. Wang, Disease dynamics in a coupled cholera model linking within-host and between-host interactions, J. Biol. Dyn., 11 (2017), 238–262. https://doi.org/10.1080/17513758.2016.1231850 doi: 10.1080/17513758.2016.1231850
    [17] C. Ratchford, J. Wang, Modeling cholera dynamics at multiple scales: environmental evolution, between-host transmission, and within-host interaction, Math. Biosci. Eng., 16 (2019), 782–812. https://doi.org/10.3934/mbe.2019037 doi: 10.3934/mbe.2019037
    [18] J. M. Drake, A. M. Kramer, Allee effects, Nat. Educ. Knowl., 3 (2011), 2.
    [19] W. C. Allee, Animal aggregations, Nature, 128 (1931), 940–941. https://doi.org/10.1038/128940b0 doi: 10.1038/128940b0
    [20] R. B. Kaul, A. M. Kramer, F. C. Dobbs, J. M. Drake, Experimental demonstration of an Allee effect in microbial populations, Biol. Lett., 12 (2016), 20160070. https://doi.org/10.1098/rsbl.2016.0070 doi: 10.1098/rsbl.2016.0070
    [21] M. Jemielita, N. S. Wingreen, B. L. Bassler, Quorum sensing controls vibrio cholerae multicellular aggregate formation, eLife, 7 (2018), e42057. https://doi.org/10.7554/eLife.42057 doi: 10.7554/eLife.42057
    [22] S. Almagro-Moreno, K. Pruss, R. K. Taylor, Intestinal colonization dynamics of Vibrio cholerae, PLoS Pathog., 11 (2015), e1004787. https://doi.org/10.1371/journal.ppat.1004787 doi: 10.1371/journal.ppat.1004787
    [23] E. J. Nelson, J. B. Harris, J. G. Morris, S. B. Calderwood, A. Camilli, Cholera transmission: the host, pathogen and bacteriophage dynamic, Nat. Rev. Microbiol., 7 (2009), 693–702. https://doi.org/10.1038/nrmicro2204 doi: 10.1038/nrmicro2204
    [24] N. Chaffey, Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walter, P. Molecular biology of the cell. 4th edn., Ann. Bot., 91 (2003), 401. https://doi.org/10.1093/aob/mcg023 doi: 10.1093/aob/mcg023
    [25] C. Kuehn, Multiple Time Scale Dynamics, Springer-Verlag, Berlin, 2015. https://doi.org/10.1007/978-3-319-12316-5
    [26] J. Müller, C. Kuttler, Methods and Models in Mathematical Biology, Springer-Verlag, Berlin, 2015. https://doi.org/10.1007/978-3-642-27251-6
    [27] R. Bertram, J. E. Rubin, Multi-timescale systems and fast-slow analysis, Math. Biosci., 287 (2017), 105–121. https://doi.org/10.1016/j.mbs.2016.07.003 doi: 10.1016/j.mbs.2016.07.003
    [28] J. A. J. Metz, O. Diekmann, The Dynamics of Physiologically Structured Populations, Springer-Verlag, Berlin, 1986. https://doi.org/10.1007/978-3-662-13159-6
    [29] O. Diekmann, M. Gyllenberg, J. Metz, Physiologically structured population models: towards a general mathematical theory, in Mathematics for Ecology and Environmental Sciences, Springer-Verlag, Berlin, (2007), 5–20. https://doi.org/10.1007/978-3-540-34428-5_2
    [30] J. M. Cushing, An Introduction to Structured Population Dynamics, SIAM, 1998. https://doi.org/10.1137/1.9781611970005
    [31] P. Magal, S. Ruan, Structured Population Models in Biology and Epidemiology, Springer, 2008. https://doi.org/10.1007/978-3-540-78273-5
    [32] O. Angulo, F. Milner, L. Sega, A SIR epidemic model structured by immunological variables, J. Biol. Syst., 21 (2013), 1340013. https://doi.org/10.1142/S0218339013400135 doi: 10.1142/S0218339013400135
    [33] M. Martcheva, S. S. Pilyugin, An epidemic model structured by host immunity, J. Biol. Syst., 14 (2006), 185–203. https://doi.org/10.1142/S0218339006001787 doi: 10.1142/S0218339006001787
    [34] À. Calsina, J. Saldaña, A model of physiologically structured population dynamics with a nonlinear individual growth rate, J. Math. Biol., 33 (1995), 335–364. https://doi.org/10.1007/BF00176377 doi: 10.1007/BF00176377
    [35] G. F. Webb, Theory of Nonlinear Age-Dependent Population Dynamics, CRC Press, 1985.
    [36] M. Y. Kim, F. A. Milner, A mathematical model of epidemics with screening and variable infectivity, Math. Comput. Modell., 21 (1995), 29–42. https://doi.org/10.1016/0895-7177(95)00029-2 doi: 10.1016/0895-7177(95)00029-2
    [37] N. Kato, H. Torikata, Local existence for a general model of size-dependent population dynamics, Abstr. Appl. Anal., 2 (1997), 207–226. https://doi.org/10.1155/s1085337597000353 doi: 10.1155/s1085337597000353
    [38] O. Diekmann, J. A. P. Heesterbeek, J. A. J. Metz, On the definition and the computation of the basic reproduction ratio R0 in models for infectious diseases in heterogeneous populations, J. Math. Biol., 28 (1990), 365–382. https://doi.org/10.1007/BF00178324 doi: 10.1007/BF00178324
    [39] H. Inaba, Age-Structured Population Dynamics in Demography and Epidemiology, Springer, 2017. https://doi.org/10.1007/978-981-10-0188-8
    [40] M. Martcheva, H. R. Thieme, Progression age enhanced backward bifurcation in an epidemic model with super-infection, J. Math. Biol., 46 (2003), 385–424. https://doi.org/10.1007/s00285-002-0181-7 doi: 10.1007/s00285-002-0181-7
    [41] A. N. Gillman, A. Mahmutovic, P. A. zur Wiesch, S. Abel, The infectious dose shapes vibrio cholerae within-host dynamics, mSystems, 6 (2021), e0065921. https://doi.org/10.1128/msystems.00659-21 doi: 10.1128/msystems.00659-21
    [42] M. Gyllenberg, Mathematical aspects of physiologically structured populations: the contributions of J. A. J. Metz, J. Biol. Dyn., 1 (2007), 3–44. https://doi.org/10.1080/17513750601032737 doi: 10.1080/17513750601032737
    [43] J. H. Tien, D. J. D. Earn, Multiple transmission pathways and disease dynamics in a waterborne pathogen model, Bull. Math. Biol., 72 (2010), 1506–1533. https://doi.org/10.1007/s11538-010-9507-6 doi: 10.1007/s11538-010-9507-6
    [44] J. Wang, C. Modnak, Modeling cholera dynamics with controls, Can. Appl. Math. Q., 19 (2011), 255–273.
    [45] R. L. M. Neilan, E. Schaefer, H. Gaff, K. R. Fister, S. Lenhart, Modeling optimal intervention strategies for cholera, Bull. Math. Biol., 72 (2010), 2004–2018. https://doi.org/10.1007/s11538-010-9521-8 doi: 10.1007/s11538-010-9521-8
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