Location: Infectious Bacterial Diseases ResearchTitle: An Immuno-epidemiological model for Johne's disease in cattle Author
|Martcheva, Maia - University Of Florida|
|Lenhart, Suzanne - University Of Tennessee|
|Eda, Shigetoshi - University Of Tennessee|
|Klinkenberg, Don - Utrecht University|
|Momotani, Eiichi - Tohto College Of Health Sciences|
Submitted to: Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/9/2015
Publication Date: 6/19/2015
Citation: Martcheva, M., Lenhart, S., Eda, S., Klinkenberg, D., Momotani, E., Stabel, J.R. 2015. An Immuno-epidemiological model for Johne's disease in cattle. Veterinary Research. doi: 10.1186/s13567-015-0190-3.
Interpretive Summary: Johne's disease is a chronic, debilitating intestinal disorder in cattle characterized by diarrhea, reduced feed intake, weight loss and death. Cattle usually become infected as young calves by ingesting feces containing the causative bacteria. However, symptoms of disease do not usually present themselves until the animals reach 3 to 5 years of age or even older. During this time the animal is infected and may be shedding the organism in its feces without showing any clinical signs of disease. In addition to reduced milk production by these animals, they also present a potential infective threat to the rest of the herd. Host immune responses to Johne’s disease are dynamic and change during the progression of disease from a latent, asymptomatic stage to a more advanced stage demonstrating symptoms listed above. Modeling the immune responses of the host during infection will help us understand how the disease progresses. This paper develops a model to explain the dynamics of the infection process and how shedding of the bacteria in the feces is impacted. Understanding the host immune response to this pathogen will help us develop control measures to prevent the spread of infection.
Technical 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.