Carotenoid-based plumage coloration predicts resistance to a novel parasite in the house finch.

The Hamilton-Zuk hypothesis proposes that the bright colours displayed by many species of birds serve as signals of individual resistance to parasites. Despite the popularity of this hypothesis, only one previous study has tested whether plumage coloration predicts how individuals respond to a disease challenge. We inoculated 24 male house finches (Carpodacus mexicanus) of variable plumage hue with a novel bacterial pathogen, Mycoplasma gallicepticum (MG). We found no relationship between plumage hue and time to first symptoms following inoculation, but we found a significant negative relationship between plumage hue and clearance of disease: males with redder plumage cleared MG infection significantly better than did males with yellower plumage. The hue of carotenoid-based plumage coloration has been shown to be a primary criterion in female mate choice in the house finch. These observations suggest that one benefit to females for choosing redder males is obtaining mates with better resistance to parasites.

The effect of mycoplasmosis on carotenoid plumage coloration in male house finches.

Parasites are widely assumed to cause reduced expression of ornamental plumage coloration, but few experimental studies have tested this hypothesis. We captured young male house finches Carpodacus mexicanus in Alabama before fall molt and randomly divided them into two groups. One group was infected with the bacterial pathogen Mycoplasma gallicepticum (MG) and the other group was maintained free of MG infection. All birds were maintained through molt on a diet of seeds with tangerine juice added to their water as a source of beta-cryptoxanthin, the natural precursor to the primary red carotenoid pigment in house finch plumage. All males grew drab plumage, but males with MG infection grew feathers that were significantly less red (more yellow), less saturated, and less bright than males that were not infected. MG targets upper respiratory and ocular tissue. Our observations show that a pathogen that does not directly disrupt carotenoid absorption or transportation can still have a significant effect on carotenoid utilization.

Susceptibility of a naïve population of house finches to Mycoplasma gallisepticum.

Since 1994 an epidemic of mycoplasmal conjunctivitis has spread throughout the eastern house finch (Carpodacus mexicanus) population leading to a significant decline in this population. The infection has not yet been reported from house finch populations west of the Great Plains. We hypothesized that the western population, like the eastern population, is susceptible to infection, and we tested this hypothesis by experimentally infecting house finches from Missoula, Montana (USA) with the house finch strain of Mycoplasma gallisepticum (MG). We compared the response of finches from Montana infected with MG to that of finches from Auburn, Alabama (USA) (October 1999-February 2000). Fifteen house finches from Montana were shipped to Auburn and quarantined for 6 wk at the Auburn University aviary. All birds were negative for MG antibodies when tested by serum plate agglutination assay and MG could not be detected in any bird by polymerase chain reaction. We tested two methods of inoculation, ocular inoculation and contact exposure to an infected finch. Seven house finches from Montana and four house finches from Alabama were infected by bilateral ocular inoculation with 20 microliters of a culture containing 1 x 10(6) color changing units of the house finch strain of MG. The remaining eight house finches from Montana were co-housed with a house finch from Alabama exhibiting mycoplasmal conjunctivitis. After exposure to the pathogen, all house finches became infected, regardless of origin or method of exposure, and all developed conjunctivitis. All birds seroconverted, and evidence of infection could be detected in every bird at some point during the course of disease. Our results suggest that house finches from the western United States are highly susceptible to infection with the house finch strain of MG.