Although studies on Plasmodium infections of wild birds have been reported frequently in the literature, our knowledge of the ecology of these parasites remains incomplete. A synthesis of data and ideas from these field studies, and recent experimental work led to the construction of the following hypothetical model for the ecology of avian malaria:

During the late spring, summer, and early fall susceptible birds (young of the year or previously uninfected adults) contract the infection from the bite of an infected mosquito on the breeding ground. The birds migrate or remain in the area and infections become latent over the winter. In the spring, migratory birds return to the breeding area and all birds commence reproductive activity. With the onset of migration and breeding activity, parasite populations become elevated in the birds. This relapse of malarial infections coincides with emergence of vectors. The mosquitoes obtain the parasite, passing it on to susceptibles in the population (whose numbers are simultaneously increasing as the result of reproduction), and the cycle continues. Under favorable conditions, transmission rates equal or exceed a level needed to replace mortality of infected birds. Under unfavorable conditions the parasite is maintained by the bird reservoir, the population of susceptibles increases, and transmission is postponed until favorable conditions return and transmission to the expanded population of susceptibles replenishes the supply of infected adults. Such a cycle, in which the parasite, vector, and susceptible host populations reach a maximum in an apparently favorable sequence, with provision for occasional failure of transmission, has obvious survival value.

A more complete understanding of the ecology of avian malaria will be achieved with the investigation of specific problem areas defined in this model. The model may prove of additional value in suggesting an ecological approach to our understanding of the epidemiology of human malarias. It may also have applicability in other disease systems where bird-mosquito relationships are similar, such as certain of the arboviruses.

Serum samples were obtained from 307 birds collected on a sheep range (Hopland Field Station) in northern California. Forty (13%) of these birds had agglutinating antibodies to Coxiella burnetii. At a nearby dairy farm, sera from 49 of 129 (38%) birds tested were positive for Q fever antibodies. In both areas the birds with the highest antibody prevalence were the carrion eating birds (crows, ravens and turkeyvultures) and those birds (Brewer's and red-winged blackbirds, golden-crowned sparrows and pigeons) that live and feed in close proximity to infected livestock. The extent to which migratory birds are involved in the ecology of this zoonosis is uncertain. Immigrant birds may have been exposed to Q fever prior to their arrival in the area; however, emigrating birds have the potential to disperse the rickettsiae from such areas where livestock are infected with C. burnetii.

Two isolations of the Montana snowshoe hare serotype of the California encephalitis virus group were made in the summer of 1968 from materials collected at Rochester, Alberta, Canada. One isolation was made from the blood of a snowshoe hare approximately 24-days old while the other was from a pool of unengorged Aedes communis group mosquitoes. The isolation of the agent from mosquitoes demonstrates the continued endemicity of the virus in the area. The recovery of the virus from the hare represents the second time a California encephalitis virus has been recovered from a snowshoe hare and relates the virus recovered from the mosquito to the known serology of the virus in hares.

A field population of English sparrows (Passer domesticus) was used to test the hypothesis that the reported spring maximum in the prevalence of Plasmodium infections is the result of an elevation of circulating parasite populations in established infections. Sparrows were captured, banded, infected with Plasmodium relictum, and released. Since natural infections were negligible in this population, patent infections in recaptured birds were assumed to result from the inoculation of parasites. The primary parasitemia in the experimental birds lasted approximately 25 days, while a substantial proportion of low intensity infections persisted through 125 days. Analysis of the seasonal distribution of patent infections in birds infected 125 days or longer showed a sharp rise in both prevalence and parasitemia in the spring. This study thus supports the hypothesis that spring relapse of established infections is responsible for the high spring prevalence of Plasmodium in birds.

Bobwhite quail (Colinus virginianus) were exposed to infection of fowl cholera by housing them in a pen where experimental epornitics of fowl cholera were in progress. These bobwhites subsequently were allowed to cohabit with susceptible turkeys. None of the turkeys developed fowl cholera thereby suggesting that the bobwhite is not a vector of fowl cholera.

Bobwhites were experimentally infected with Histomonas meleagridis and Heterakis gallinarum. Chickens and turkeys were similarly infected for comparison. Although the bobwhites were nearly as susceptible to Histomonas infections as were New Hampshire chickens, and more susceptible to tissue invasion, clinical histomoniasis was much less severe than in young turkeys. The bobwhites were poor hosts for Heterakis, whether Histomonas was also present or not. Thus, it appears that bob-whites are relatively unimportant in contaminating soil with Histomonas-bearing Heterakis eggs.