Behavior and disease interact bidirectionally and on multiple levels of host organization, and these interactions can have important consequences for population-level disease dynamics. I explored how behavior can both influence and respond to infectious disease in a banded mongoose population experiencing epidemics of tuberculosis (TB) caused by the bacterial pathogen Mycobacterium mungi in the M. tuberculosis complex (Alexander et al. 2010). Banded mongooses are highly social carnivores that live in troops of 5 to 65 individuals. Mycobacterium mungi appears to be primarily environmentally transmitted, but direct horizontal transmission cannot be ruled out. Approximately 10-20% of mongooses become diseased with TB each year in the study population in and around Chobe National Park, Botswana, and all mongooses with clinical signs of TB die within months. Characteristics of both banded mongooses and clinical TB provided a productive study system for exploring interactions between behavior and disease: first, free-living mongooses can be habituated and directly observed; second, the clinical signs of TB can be visually assessed non-invasively; and third, the mongooses' high sociality and egalitarianism provide a unique and ecologically relevant host social system for examining bidirectional interactions between behavior and infectious disease.
I found that banded mongooses influenced and responded to disease through their behavior at both the individual and troop level, with possible implications for banded mongoose population and disease dynamics. Due to the environmental transmission of M. mungi, which appears to invade mongooses through breaks in the skin and nasal planum (Alexander et al. 2010), I focused on aggressive interactions as a potential risk factor for acquiring TB in this system. Troops with higher levels of aggression had more injuries, and at the individual level, injuries were a strong predictor of TB, suggesting that aggression may increase risk of disease by creating potential invasion sites for the pathogen. Troops were more aggressive when they foraged in garbage than when they foraged in other habitats, presumably due to the concentration of resources at this highly modified habitat. Overall, my results on how behavior can influence disease in this system suggest that anthropogenic supplementation of food, albeit inadvertent in this system, augments aggression levels in banded mongooses and may in turn lead to a higher incidence of TB.
Second, I examined how behavior responds to disease in banded mongooses. Diseased individuals showed significantly lower activity and alertness, but intriguingly, did not show a reduction in overall social behaviors. Diseased individuals were less likely to disperse than healthy individuals, and healthy individuals with diseased troopmates may have been more likely to disperse than individuals without diseased troopmates. Despite this latter possible increase in dispersal in the presence of diseased conspecifics, diseased individuals were not avoided by their troopmates in daily social interactions. For example, diseased individuals were allogroomed at a higher than expected rate even though their reciprocation during allogrooming was approximately half that of healthy individuals.
These interactions between behavior and disease have implications for banded mongoose troop and population dynamics, via changes in dispersal behavior and mortality, and can also affect disease dynamics, such as transmission rate. For example, changes to dispersal may affect the amount of inbreeding and outbreeding that occurs in this normally inbred species, and disease might be amplified in areas where aggression is increased by resource augmentation from humans. Additionally, the role that garbage plays in mongoose aggression suggests that humans may be inadvertently increasing disease incidence in this system, as well as in other taxa for which anthropogenic food augmentation may alter disease dynamics via changes in intraspecific aggression. This research sheds light on ways that behavior can influence and respond to disease that are often overlooked in disease ecology. / Ph. D.
| Identifer | oai:union.ndltd.org:VTETD/oai:vtechworks.lib.vt.edu:10919/52868 |
| Date | 04 September 2013 |
| Creators | Fairbanks, Bonnie Marie |
| Contributors | Biological Sciences, Hawley, Dana M., Alexander, Kathleen A., Moore, Ignacio T., Walters, Jeffrey R., Hopkins, William A. |
| Publisher | Virginia Tech |
| Source Sets | Virginia Tech Theses and Dissertation |
| Detected Language | English |
| Type | Dissertation |
| Format | ETD, application/pdf, text/plain |
| Rights | In Copyright, http://rightsstatements.org/vocab/InC/1.0/ |
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