An immuno-epidemiological model for Johne's disease in cattle.

Maia Martcheva,Shigetoshi Eda,Eiichi Momotani,Judy Stabel,Suzanne Lenhart,Don Klinkenberg

doi:10.1186/s13567-015-0190-3

Abstract

To better understand the mechanisms involved in the dynamics of Johne’s disease in dairy cattle, this paper illustrates a novel way to link a within-host model for Mycobacterium avium ssp. paratuberculosis with an epidemiological model. The underlying variable in the within-host model is the time since infection. Two compartments, infected macrophages and T cells, of the within-host model feed into the epidemiological model through the direct transmission rate, disease-induced mortality rate, the vertical transmission rate, and the shedding of MAP into the environment. The epidemiological reproduction number depends on the within-host bacteria load in a complex way, exhibiting multiple peaks. A possible mechanism to account for the switch in shedding patterns of the bacteria in this disease is included in the within-host model, and its effect can be seen in the epidemiological reproduction model.

Highlights

Johne’s disease (JD) in dairy cattle is a chronic infectious disease in the intestines caused by the bacillus, Mycobacterium avium ssp. paratuberculosis (MAP)
Implications of the within-host dynamics to the epidemiology of JD Immuno-epidemiological models allow us to evaluate the impact of the within-host bacterial load on the epidemiological reproduction number
Overview of insights of immunological model The immunological model in the system describes the within-host dynamics of MAP

Summary

Introduction

Johne’s disease (JD) in dairy cattle is a chronic infectious disease in the intestines caused by the bacillus, Mycobacterium avium ssp. paratuberculosis (MAP). MAP in a contaminated environment infects cattle through oral route. Actual infection occurs when MAP bacilli are phagocytosed by M-cells covering the dome of the Peyer’s patches [1] and transported to macrophages. In the early stages of the infection, some of the MAP will not be destroyed by macrophages and will grow in those cells until cellular immunity will be generated. To develop specific cellular immunity, macrophages differentiate into epithelioid cells and intracellular growth of the MAP will be suppressed. Epithelioid cells form specific structures, granulomas, which act to restrict MAP growth inside and destroy them gradually. Some of the MAP in the granuloma will survive and enter a period of dormancy until reactivation. Reactivation of MAP will start slowly in the subclinical stage in which intermittent shedding of MAP will start.

Methods

Results

Conclusion