Sarcoptic mange caused by Sarcoptes scabiei is responsible for epizootic disease in populations of wild canids in North America, Europe and Australia, wild cats in Europe and Africa, wild ungulates and wild boars in Europe, wombats and koalas in Australia, and great apes and various wild bovids in Africa. Although short-term mortality may appear devastating, in a self-sustaining population, mortality is non-compensatory and a mange epizootic generally does not affect long-term population dynamics. Alternatively, the net effect of a mange epizootic can have serious consequences in remnant or fragmented populations of CITES-listed, threatened, or endangered species where loss of even a few individuals can be critical to the survival or restoration of a species (CITES: Convention on International Trade in Endangered Species of Wild Fauna and Flora). The pathogenesis and concordant clinical symptoms of mange depends on the immune status of the respective host.
Naïve, immunocompromised or anergic animals that are unable to evoke hypersensitivity responses develop an extensive epidermal hyperkeratosis usually without marked alopecia, but with an underlying chronic dermal inflammation and an abundance of mites in the skin. Immunocompetent hosts are able to develop strong types I and IV hypersensitivity responses that result in a marked decrease and eventual loss of mites in the skin. However, there are dramatic structural and functional changes in the skin; it becomes extensively thickened, greyish in colour and there is a marked eosinophilia throughout the epidermis and dermis. There is often almost complete alopecia. Isolation and treatment of infected individuals may be warranted, and has met with some success in small remaining populations of certain highly endangered species.