Seasonal fluctuations in infectious disease incidence are common, and have been observed for many infectious agents. Immune condition can also change seasonally due to such pathogen fluctuations, a well as to changes in other stress-inducing and immunomodulatory factors such as reproduction and lactation. In addition, most vertebrate hosts are concurrently infected with multiple pathogens, and such coinfections can interact with each other, with the immune system, and with other physiological factors to affect both the individual hosts and population dynamics. While many studies regarding the effects of coinfections and immune trade-offs have been conducted in laboratory settings, similar studies in wildlife are as yet very rare. Fewer studies have been conducted regarding disease and immune seasonality, as these are difficult to model in laboratory settings and require difficult, longitudinal studies in natural systems. In addition, most research regarding disease seasonality in natural systems that has been done has focused on the impacts of abiotic factors on pathogen and vector survival and abundance, or on population-wide dynamics, rather than on physiological mechanisms of host susceptibility. To fully understand the ecology of infectious diseases and the reasons for disease outbreaks, it is necessary to extend laboratory studies into natural hosts in natural systems, as well as to extend wildlife studies to incorporate the complex interactions between environmental, physiological, and coinfection factors. My dissertation research thus focused on the ecological immunology of infectious disease in a natural system, from physiological, seasonal, and coinfection perspectives. I examined the ability of plains zebra (Equus quagga), springbok (Antidocas marsupialis), and African elephant (Loxodonta africana) to respond immunologically to regular anthrax outbreaks in an endemic anthrax system (Etosha National Park, ENP, Namibia). I also examined how zebra and springbok macroparasite coinfections varied with and affected changes in immune parameters, stress, reproductive hormone levels, and seasonal timing of anthrax outbreaks.