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.     

Susceptibility of wild songbirds to the house finch strain of Mycoplasma gallisepticum

Conjunctivitis in house finches (Carpodacus mexicanus), caused by Mycoplasma gallisepticum (MG), was first reported in 1994 and, since this time, has become endemic in house finch populations throughout eastern North America. Although the house finch is most commonly associated with MG-related conjunctivitis, MG has been reported from other wild bird species, and conjunctivitis (not confirmed as MG related) has been reported in over 30 species. To help define the host range of the house finch strain of MG and to better understand the effect of MG on other host species, we monitored a community of wild birds for exposure to MG and conducted experimental infections on nine avian species. For the field portion of our study, we conducted a 9-mo survey (August 2001 to April 2002) of wild avian species in a peri-urban environment on the campus of Auburn University. During this time 358 birds, representing 13 different families, were sampled. No clinical signs of mycoplasmosis were observed in any bird. Thirteen species from nine families had positive agglutination reactions for antibodies to MG, but all birds tested negative by polymerase chain reaction (PCR). Three mourning doves were PCR-positive for MG, but antibodies to MG were not detected. In the experimental infections, we exposed seven native avian species and two cage-bird species to MG (May 2000 to June 2002). After exposure, clinical disease was seen in all four species from the family Fringillidae and in eastern tufted titmice (Baeolophus bicolor). In addition, three other species were infected without clinical signs, suggesting that they may represent potential MG reservoirs.     

Mycoplasmal conjunctivitis in songbirds from New York

A field study was conducted to determine the prevalence of conjunctivitis and Mycoplasma gallisepticum (MG) infections in house finches (Carpodacus mexicanus) and other songbirds common to bird feeders in Tompkins County (New York, USA). Eight hundred two individuals of 23 species and nine families of birds were captured and given physical examinations during the 14 mo study beginning in February 1998. Clinical conjunctivitis (eyelid or conjunctival swelling, erythema, and discharge) was observed in 10% (19/196) of house finches examined, and only in the winter months from November to March. Unilateral conjunctivitis was observed in 79% (15/19) of affected house finches; one case developed bilateral disease between 8 and 18 days following initial examination. Conjunctivitis was observed in a similar proportion of males and females sampled, and body condition scores and wing chord lengths were not significantly different between diseased and non-diseased house finches. Mycoplasma gallisepticum was isolated from 76% (13/17) of finches with conjunctivitis and 2% (3/168) of clinically normal house finches sampled during the study. DNA fingerprints of 11 MG isolates using random amplification of polymorphic DNA (RAPD) techniques showed no apparent differences in banding patterns over the course of the study, suggesting persistence of a single MG strain in the study population. The prevalence of conjunctivitis and MG infections declined in house finches between February/March 1998 and February/March 1999 (23% to 6%, and 20% to 5%, respectively), but only the former was significant (P < 0.05). Conjunctivitis was also observed in four American goldfinches (Carduelis tristis) and one purple finch (Carpodacus purpureus). Mycoplasma gallisepticum infection was confirmed in the purple finch, the first documented case of MG-associated conjunctivitis in this species. The purple finch isolate was similar to house finch isolates from the study site by RAPD analysis. Positive plate agglutination (PA) tests were recorded in one other goldfinch and two purple finches, suggesting exposure of these individuals to MG. Positive PA tests were also obtained from two brown-headed cowbirds (Molothrus ater) and four tufted titmice (Parus bicolor), but MG infection could not be confirmed in these cases due to lack of samples. Based on these findings, the prevalence of MG infections in hosts other than house finches appear to be low in the population sampled. There is growing evidence, however, that songbird species other than house finches are susceptible to MG infection and disease.     

Common garden experiment reveals pathogen isolate but no host genetic diversity effect on the dynamics of an emerging wildlife disease

Host genetic diversity can mediate pathogen resistance within and among populations. Here we test whether the lower prevalence of Mycoplasmal conjunctivitis in native North American house finch populations results from greater resistance to the causative agent, Mycoplasma gallisepticum (MG), than introduced, recently‐bottlenecked populations that lack genetic diversity. In a common garden experiment, we challenged wild‐caught western (native) and eastern (introduced) North American finches with a representative eastern or western MG isolate. Although introduced finches in our study had lower neutral genetic diversity than native finches, we found no support for a population‐level genetic diversity effect on host resistance. Instead we detected strong support for isolate differences: the MG isolate circulating in western house finch populations produced lower virulence, but higher pathogen loads, in both native and introduced hosts. Our results indicate that contemporary differences in host genetic diversity likely do not explain the lower conjunctivitis prevalence in native house finches, but isolate‐level differences in virulence may play an important role.     

Seasonality and wildlife disease: how seasonal birth, aggregation and variation in immunity affect the dynamics of Mycoplasma gallisepticum in house finches

We examine the role of host seasonal breeding, host seasonal social aggregation and partial immunity in affecting wildlife disease dynamics, focusing on the dynamics of house finch conjunctivitis (Mycoplasma gallisepticum (MG) in Carpodacus mexicanus). This case study of an unmanaged emerging infectious disease provides useful insight into the important role of seasonal factors in driving ongoing disease dynamics. Seasonal breeding can force recurrent epidemics through the input of fresh susceptibles, which will clearly affect a wide variety of wildlife disease dynamics. Seasonal patterns of social aggregation and foraging behaviour could change transmission dynamics. We use latitudinal variation in the timing of breeding, and social systems to model seasonal dynamics of house finch conjunctivitis across eastern North America. We quantify the patterns of seasonal breeding, and social aggregation across a latitudinal gradient in the eastern range of the house finch, supplemented with known field and laboratory information on immunity to MG in finches. We then examine the interactions of these factors in a theoretical model of disease dynamics. We find that both forms of seasonality could explain the dynamics of the house finch-MG system, and that these factors could have important effects on the dynamics of wildlife diseases generally. In particular, while either alone is sufficient to create recurrent cycles of prevalence in a population with an endemic disease, both are required to produce the specific semi-annual pattern of disease prevalence seen in the house finch conjunctivitis system.     

Characterization of the mycoplasmal conjunctivitis epizootic in a house finch population in the southeastern USA

An epidemiological study of the prevalence of mycoplasmal conjunctivitis in the house finch (Carpodacus mexicanus) was conducted in Auburn (Alabama, USA) between March 1998 and February 1999. Clinical disease was observed in 4% of the 1,214 finches trapped and examined. This rate is comparable to the average annual prevalence observed in this population since 1996, although the prevalence of clinical disease observed in the peak months of September through November was lower than in previous years. Clinically ill birds were observed in all months of the study. To estimate the prevalence of recovering and asymptomatic, infected birds, we tested a subset of 334 house finches serologically for exposure to Mycoplasma gallisepticum (MG) using the serum plate agglutination (SPA) assay. The prevalence of clinical disease in this subsample was slightly higher (7%) than in the entire sample, reflecting the fact that the serological survey was initiated in the late summer when the prevalence of MG infection peaks in our study population and a sampling bias for symptomatic birds. The serological survey indicated that 13% of this subpopulation had been exposed to MG. We also tested 46 of 334 finches by polymerase chain reaction (PCR) to detect MG in seropositive, asymptomatic birds. Use of the PCR in conjunction with the SPA detected six asymptomatic, infected birds that may represent potential carriers or birds in the early stages of infection. The decreasing prevalence of clinical disease observed during the peak months suggests a changing host-parasite relationship. Continued surveillance of this population, employing both clinical observation and serological analysis will be useful in characterizing these changes over time.     

Genotypic analyses of Mycoplasma gallisepticum isolates from songbirds by random amplification of polymorphic DNA and amplified-fragment length polymorphism

Mycoplasma gallisepticum (MG) conjunctivitis emerged in 1994 as a disease of free-ranging house finches (Carpodacus mexicanus) in North America and has also been isolated from other songbirds with conjunctivitis. Random amplification of polymorphic DNA (RAPD) of house finch and other songbird isolates has suggested that a single 'strain' initiated this outbreak. To explore the possibility of genomic variability among house finch isolates of MG and to evaluate the utility of a second technique for MG genotyping, we selected samples from our archive of reference strains and wild songbird isolates to analyze using both RAPD and amplified-fragment length polymorphism (AFLP); this is a newer technique that has been successfully used to explore the genomic variability of several Mycoplasma species. Both RAPD and AFLP results confirmed previous observations that during the initial stages of the MG epidemic in songbirds, isolates from different geographic locations and songbird species had genotypes that appeared to be highly similar, further supporting a single point source of origin. One 2001 isolate from New York was clearly different from the other songbird samples and clustered together with the vaccine and reference strains, indicating that substantial molecular evolution or a separate introduction has occurred.     

The Potential Impact of Disease on the Migratory Structure of a Partially Migratory Passerine Population

Since its introduction into eastern North America in the 1940s, the eastern population of house finches (Carpodacus mexicanus) has become partially migratory, unlike its nonmigratory source population in southern California (Able and Belthoff in Proc. R. Soc. Lond. 265 (1410), 2063–2071, 1998; Belthoff and Gauthreaux in Condor 93, 374–382, 1991). The infectious disease mycoplasmal conjunctivitis (pathogen Mycoplasma gallisepticum or “MG”), which has been monitored in the house finch population since its appearance around 1993 (Dhondt et al. in J. Wild. Dis. 34 (2), 265–280, 1998), may induce higher mortality rates among populations in more northerly latitudes relative to more southerly populations. Here, we investigate the potential impact of this differential disease mortality on the migratory structure of the eastern house finch population using an epidemic modeling approach. Analytical and computational results suggest the ongoing MG epidemic in the eastern house finch could lead to increases in the percentage of and the total number of migrating individuals in a population despite overall population declines, assuming relatively high winter mortality rates in the north eastern part of their range. These results also suggest that empirical evidence of such a change in migratory structure would be most noticeable in northerly inland populations that showed significant declines following the initial outbreak of MG in the east.     

Host Responses to Pathogen Priming in a Natural Songbird Host

Hosts in free-living populations can experience substantial variation in the frequency and dose of pathogen exposure, which can alter disease progression and protection from future exposures. In the house finch–Mycoplasma gallisepticum (MG) system, the pathogen is primarily transmitted via bird feeders, and some birds may be exposed to frequent low doses of MG while foraging. Here we experimentally determined how low dose, repeated exposures of house finches to MG influence host responses and protection from secondary high-dose challenge. MG-naive house finches were given priming exposures that varied in dose and total number. After quantifying host responses to priming exposures, all birds were given a secondary high-dose challenge to assess immunological protection. Dose, but not the number of exposures, significantly predicted both infection and disease severity following priming exposure. Furthermore, individuals given higher priming doses showed stronger protection upon secondary, high-dose challenge. However, even single low-dose exposures to MG, a proxy for what some birds likely experience in the wild while feeding, provided significant protection against a high-dose challenge. Our results suggest that bird feeders, which serve as sources of infection in the wild, may in some cases act as “immunizers,” with important consequences for disease dynamics.     

Further western spread of Mycoplasma gallisepticum infection of house finches

Mycoplasma gallisepticum, an important pathogen of poultry, especially chickens and turkeys, emerged in 1994 as the cause of conjunctivitis in house finches (Carpodacus mexicanus) in their eastern range of North America. The resulting epidemic of M. gallisepticum conjunctivitis severely decreased house finch abundance and the continuing endemic disease in the eastern range has been associated with repeating seasonal peaks of conjunctivitis and limitation of host populations. Mycoplasma gallisepticum conjunctivitis was first confirmed in the western native range of house finches in 2002 in a Missoula, Montana, population. Herein, we report further western expansion of M. gallisepticum conjunctivitis in the native range of house finches based on positive polymerase chain reaction results with samples from birds captured in 2004 and 2005 near Portland, Oregon.     

Reconciling molecular signatures across markers: mitochondrial DNA confirms founder effect in invasive North American house finches (<Emphasis Type="Italic">Carpodacus mexicanus</Emphasis>)

Well-characterized species introductions provide opportunities to compare the genetic signatures of known founder effects across classes of molecular markers. The release of small numbers of house finches (Carpodacus mexicanus) into the eastern United States in the 1940s led to substantial interest in the effects of this introduction on genetic diversity in this now abundant species, an issue that has been highlighted by a recent Mycoplasma disease epidemic that most intensively affects the introduced and potentially genetically depauperate house finch populations. Previous studies comparing genetic diversity levels in native and introduced house finch populations produced seemingly disparate results: comparisons based on amplified fragment length polymorphism, RFLP mtDNA, and allozyme markers found essentially equivalent levels of diversity in eastern and western populations, whereas microsatellite markers showed clear reductions in diversity in the introduced populations. Here we employ sequence variation at the ND2 mtDNA locus to further compare levels of diversity between the four native and five introduced house finch populations that were previously examined in the microsatellite study. We found substantially lower ND2 haplotype richness and diversity across all introduced populations of house finches. The majority of sequence variation (78%) was detected within subpopulations, with the remainder (22%) explained by the historical status of each population (native or introduced). Our results are consistent with previous microsatellite evidence for a founder effect during the introduction of eastern house finches, and suggest that the mtDNA founder effect was particularly severe, likely owing to a male-biased sex ratio at the time of introduction coupled with the lower effective population size of clonally inherited markers. We discuss how the inconsistencies between past studies of house finch diversity can inform the usefulness of distinct marker sets for detecting molecular signatures of founder events.     

Genetic diversity predicts pathogen resistance and cell-mediated immunocompetence in house finches

Evidence is accumulating that genetic variation within individual hosts can influence their susceptibility to pathogens. However, there have been few opportunities to experimentally test this relationship, particularly within outbred populations of non-domestic vertebrates. We performed a standardized pathogen challenge in house finches (Carpodacus mexicanus) to test whether multilocus heterozygosity across 12 microsatellite loci predicts resistance to a recently emerged strain of the bacterial pathogen, Mycoplasma gallisepticum (MG). We simultaneously tested whether the relationship between heterozygosity and pathogen susceptibility is mediated by differences in cell-mediated or humoral immunocompetence. We inoculated 40 house finches with MG under identical conditions and assayed both humoral and cell-mediated components of the immune response. Heterozygous house finches developed less severe disease when infected with MG, and they mounted stronger cell-mediated immune responses to phytohaemagglutinin. Differences in cell-mediated immunocompetence may, therefore, partly explain why more heterozygous house finches show greater resistance to MG. Overall, our results underscore the importance of multilocus heterozygosity for individual pathogen resistance and immunity.     

Host range and dynamics of mycoplasmal conjunctivitis among birds in North America

An epidemic of conjunctivitis among house finches (Carpodacus mexicanus) caused by Mycoplasma gallisepticum (MG) bacterial infections was first described in 1994. The disease exhibits high primary host specificity, but has been isolated from a limited number of secondary avian hosts at various times and locations. We used records from the House Finch Disease Survey, a continent-wide, volunteer monitoring project, to document the host range of conjunctivitis in birds at feeding stations and to investigate how disease in house finches might influence the spread of conjunctivitis to other hosts. Between 1994 and 1998, participants recorded 675 cases of conjunctivitis in 31 species other than house finches in eastern North America. Seventy five % of these cases were observed among three species: American goldfinches (Carduelis tristis), purple finches (Carpodacus purpureus) and house sparrows (Passer domesticus). The proportion of sites with diseased wintering populations of the three species increased over the 4 yr study and coincided with range expansion of conjunctivitis in house finches. Sites with diseased house finches present were significantly more likely to report conjunctivitis in each of the three species during the same month. These observations are most consistent with transmission of an infectious agent (presumably MG) from house finches to these secondary hosts via spillover of localized epidemics, rather than sustained interspecific transmission.     

Prevalence of Blood Parasites in Eastern Versus Western House Finches: Are Eastern Birds Resistant to Infection?

The rapid spread of the bacterial disease, Mycoplasma gallisepticum (MG), throughout the introduced range of house finches (Carpodacus mexicanus) in eastern North America, compared to its slower spread through the native western range, has puzzled researchers and highlights the need to understand the relative differences in health state of finches from both populations. We conducted a light-microscope survey of hemoparasites in populations of finches from Arizona (within the western range) and from Alabama (within the eastern range), and compared our estimates of prevalence to published reports from house finches sampled in both ranges. Of the 33 Arizona birds examined, we recorded hematozoan infections in 16 (48.5%) individuals, compared to 1 infected Alabama bird out of 30 birds examined (3.3%). Based on independent surveys of seven western North American and five eastern North American populations of house finches the average prevalence of blood parasites in western populations is 38.8% (±17.9 SD), while the average prevalence within the eastern range is only 5.9% (±6.1 SD). The average rate of infection among all songbirds sampled in the east is 34.2% (±4.8 SD). Thus, our surveys of wild birds as well as previously published observations point to eastern house finches having a much lower prevalence of blood parasite infections than their western counterparts. Combined with the fact that eastern finches also tend to have lower rates of avian pox infections than do western birds (based on a literature review), these observations suggest that eastern birds have either strong resistance to these infections or high susceptibility and associated mortality.     

Diagnosis and treatment of conjunctivitis in house finches associated with mycoplasmosis in Minnesota

An ongoing outbreak of Mycoplasma gallisepticum-associated conjunctivitis in house finches (Carpodacus mexicanus) that began in 1994 in the eastern United States has been spreading westward. House finches presenting with the clinical signs of M. gallisepticum-associated conjunctivitis were first seen at the Wildlife Rehabilitation Center of Minnesota (Minnesota, USA) in July of 1996, and 42 cases were admitted from 26 December 1996 to 10 August 1997. A nested PCR was designed for sensitive and specific detection of the presence of the organism. Twelve birds were treated with oral enrofloxacin (15 mg/kg, twice daily for 21 days) and ophthalmic gentamicin (twice daily for 21 days). All treated birds showed resolution of clinical signs. Following treatment, finches were held for up to 6 mo and tested for the presence of M. gallisepticum by culture and nested polymerase chain reaction (PCR). Eight of twelve finches (67%) were positive for M. gallisepticum by nested-PCR and four (33%) were positive by culture. The results suggest that oral enrofloxacin and opthalmic gentamicin are not an effective treatment for the eradication of M. gallisepticum in house finches. Further, the results show that nested PCR is an effective method for detection of M. gallisepticum in house finches and was more sensitive than culture.     

Ketocarotenoid circulation,but not retinal carotenoid accumulation,is linked to eye disease status in a wild songbird

Pathogenic or parasitic infections pose numerous physiological challenges to organisms. Carotenoid pigments have often been used as biomarkers of disease state and impact because they integrate multiple aspects of an individual’s condition and nutritional and health state. Some diseases are known to influence carotenoid uptake from food (e.g. coccidiosis) and carotenoid use (e.g. as antioxidants/immunostimulants in the body, or for sexually attractive coloration), but there is relatively little information in animals about how different types of carotenoids from different tissue sources may be affected by disease. Here we tracked carotenoid accumulation in two body pools (retina and plasma) as a function of disease state in free-ranging house finches (Haemorhous mexicanus). House finches in eastern North America can contract mycoplasmal conjunctivitis (Mycoplasma gallisepticum, or MG), which can progress from eye swelling to eye closure and death. Previous work showed that systemic immune challenges in house finches lower carotenoid levels in retina, where they act as photoprotectors and visual filters. We assessed carotenoid levels during the molt period, a time of year when finches uniquely metabolize ketocarotenoids (e.g. 3-hydroxy-echinenone) for acquisition of sexually selected red plumage coloration, and found that males infected with MG circulated significantly lower levels of 3-hydroxy-echinenone, but no other plasma carotenoid types, than birds exhibiting no MG symptoms. This result uncovers a key biochemical mechanism for the documented detrimental effect of MG on plumage redness in H. mexicanus. In contrast, we failed to find a relationship between MG infection status and retinal carotenoid concentrations. Thus, we reveal differential effects of an infectious eye disease on carotenoid types and tissue pools in a wild songbird. At least compared to retinal sources (which appear somewhat more temporally stable than other body carotenoid pools, even to diseases of the eye evidently), our results point to either a high physiological cost of ketocarotenoid synthesis (as is argued in models of sexually selected carotenoid coloration) or high benefit of using this ketocarotenoid to combat infection.     

Re-exposure of captive house finches that recovered from Mycoplasma gallisepticum infection

Fourteen house finches were reinoculated (re-exposed) with 0.05 ml (3.24x10(5) colony forming units/ml) of Mycoplasma gallisepticum (MG) in the conjunctival sac of each eye. All birds used in this reinoculation study had recovered from previous infection between 27 and 83 days after inoculation. Recovery was based on the absence of clinical signs of conjunctivitis and/ or the inability to detect MG in conjunctival or choanal samples. Birds were maintained in individual cages under controlled environmental conditions at temperature 21-24 C, relative humidity 70%, and a light cycle adjusted to ambient values. They were divided into three groups, (A, B, and C). Five birds each were reinoculated 219 days (7.3 mo, group A) and 314 days (10.47 mo, group B) after the original infection. The final group of four birds was reinoculated at 425 days after experimental infection (14.17 mo, group C). Although the birds were randomly assigned to the three groups, the duration of the disease state (number of days until clinical signs last observed) during initial infection differed: group A mean=37.0+/-SE 4.549, group B mean=63.6+/-SE 6.306, group C mean=42.75+/-SE 2.750; analysis of variance F2,11=8.17, P=0.007. Within 24 hr after reinoculation six of the 14 experimental birds had developed some clinical signs of MG-induced conjunctivitis. At 3 days after reinoculation, 12 of the 14 birds had unilateral or bilateral conjunctivitis. The duration of clinical signs in the reinoculated individuals was significantly shorter than with their previous infection. These results suggest that the birds were able to mount a rapid and strong immune response following re-exposure. However, they were susceptible to reinfection and developed disease, suggesting that reinfection or perhaps even recurrence of infection and disease could occur in the free-ranging population. This may represent an important component in the epidemiology of this disease in house finches.     

Dynamics of Mycoplasmal Conjunctivitis in the Native and Introduced Range of the Host

In 1994, Mycoplasma gallisepticum, a common bacterial poultry pathogen, caused an epidemic in house finches in the eastern part of their North American range where the species had been introduced in the 1940s. Birds with mycoplasmal conjunctivitis were reported across the entire eastern United States within 3–4 years. Here we track the course of the Mycoplasma gallisepticum epidemic as it reached native, western North American populations of the house finch. In 2002, Mycoplasma gallisepticum was first observed in a native house finch population in Missoula, MT, where it gradually increased in prevalence during the next 2 years. Concurrently, house finches with conjunctivitis were reported with increasing number in the Pacific Northwest. In native populations of the host, the epidemic expanded more slowly, and reached lower levels of prevalence than in the eastern, introduced range of the species. Maximal prevalence was about half in the Missoula population than in local populations in the East. Although many factors can contribute to these differences, we argue that it is most likely the higher genetic heterogeneity in western than in eastern populations caused the lower impact of the pathogen.     

Spatial Variation in an Avian Host Community: Implications for Disease Dynamics

Because many pathogens can infect multiple host species within a community, disease dynamics in a focal host species can be affected by the composition of the host community. We examine the extent to which spatial variation in species’ abundances in an avian host community may contribute to geographically varying prevalence of a recently emerged wildlife pathogen. Mycoplasma gallisepticum is a pathogen novel to songbirds that has caused substantial mortality in house finches (Carpodacus mexicanus) in eastern North America. Though the house finch is the primary host species for M. gallisepticum, the American goldfinch (Spinus tristis) and northern cardinal (Cardinalis cardinalis) are alternate hosts, and laboratory experiments have demonstrated M. gallisepticum transmission between house finches and goldfinches. Still unknown is the real world impact on disease dynamics of variation in abundances of the three hosts. We analyzed data from winter-long bird and disease surveys in the northeastern United States. We found that higher disease prevalence in house finches was associated with higher numbers of northern cardinals and American goldfinches, although only the effect of cardinal abundance was statistically significant. Nevertheless, our results indicate that spatial variation in bird communities has the potential to cause geographic variation in disease prevalence in house finches.