Spatial spread of an emerging infectious disease: Conjunctivitis in House Finches.
Reviewed 09/09/10
The authors of this paper present work conducted on the emergence of an introduced pathogen in House Finch populations. Mycoplasma gallisepticum (MG) is a bacteria that produces conjunctivitis in house finches,the infection symptoms in the birds were first noted in 1993-1994. Uniquely the host population also represents a long term invasive in the continental US; house finches were traditionally only found in the Western US until a point introduction in New York around 1940. Bird invasion is fundamentally different from animal invasive studies because their seasonal migration patterns violate the requirements of diffusion theory, which can be used to model invasion. Except at extremely high prevalence of MG in the house finch population, the pathogen attacks only one focal host.
The data was collected by amateur bird watchers who noted presence-absence of both infected and uninfected finches at their backyard birdfeeders. This data was than aggregated to county wide 'grid cells' across states up and down the Eastern US.
A logistic regression model was fit with parameters for observer effort, land use, regional presence of disease in recent past, and host migration.Prevalence of disease was calculated from a days observed perspective and not from total observations of finches so as to reduce inaccuracy of observer efforts.
The data showed an initially linear increase in the spread of the disease, consistent with diffusion theory, but then began to cap out, conceivably as the optimal novel environments for the disease to infect its host dwindled. This result is posited as a condition for diffusion theory to be applicable: that the invader (MG in this case) can not experience an Allee effect due to initial low abundance, and that the linear trend will continue as long as their is a high degree of optimal new territory in which the spread can occur. For MG the decrease in the velocity of the spread may be due to a decline in human dense-suburban environments, where their host, the house finch, is itself most commonly found. The disease was marginalized at the edges of its host population.
The house finch invasion was however most limited by its initially small population after introduction and has only more recently begun to accelerate its spread.
The data available for seasonal trends in the disease spread was perhaps the most interesting part of the article however. Deviance from the predicted trend showed that peak prevalence in disease occurred in the summer breeding season up to October, the time when finches come together for southward migration, with a smaller peak in prevalence noted in early spring, a time when the bird population is also experiencing some regional dispersal movements.
The complex nature of the seasonal movement of the birds is matched by the complexity of the spread rates f the disease over the year. Time lags due to regional prevalence do not fit into simply definable categories. Rising disease trends in one part of the year had effects on later months, and were themselves affected by earlier trends in the year. For example, the month of July had low overall disease prevalence, but was at the start of a rising seasonal trend in prevalence.This is linked with the key early dispersal of juvenile finches.
The biggest query I had with the authors methods was their reliance on data to model disease prevalence that was based on the fact that symptoms were easily observable and traceable in the host population. However, at the end of the paper they draw key conclusions as to the regard of asymptomatic individuals that may be driving future disease spread even in non-peak seasons of the disease. This they say is the reason why seasonal trends in general were important in their model, but no single month alone was deemed critical.
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