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Anthropogenic food provisioning of wildlife can alter the frequency of contacts among hosts and between hosts and environmental sources of pathogens. Despite the popularity of garden bird feeding, few studies have addressed how feeders influence host contact rates and disease dynamics. We experimentally manipulated feeder density in replicate aviaries containing captive, pathogen-naive, groups of house finches ( Haemorhous mexicanus ) and continuously tracked behaviours at feeders using radio-frequency identification devices. We then inoculated one bird per group with Mycoplasma gallisepticum (Mg), a common bacterial pathogen for which feeders are fomites of transmission, and assessed effects of feeder density on house finch behaviour and pathogen transmission. We found that pathogen transmission was significantly higher in groups with the highest density of bird feeders, despite a significantly lower rate of intraspecific aggressive interactions relative to the low feeder density groups. Conversely, among naive group members that never showed signs of disease, we saw significantly higher concentrations of Mg-specific antibodies in low feeder density groups, suggesting that birds in low feeder density treatments had exposure to subclinical doses of Mg. We discuss ways in which the density of garden bird feeders could play an important role in mediating the intensity of Mg epidemics.This article is part of the theme issue 'Anthropogenic resource subsidies and host-parasite dynamics in wildlife'., (© 2018 The Author(s).)

Tests for the presence of pathogen DNA or antibodies are routinely used to survey for current or past infections. In diseases that emerge following a host jump estimates of infection rate might be under- or overestimated. We here examine whether observed rates of infection are biased for a non-focal host species in a model system. The bacterium Mycoplasma gallisepticum is a widespread pathogen in house finches (Haemorhous mexicanus), a fringillid finch, but an unknown proportion of individuals of other songbird species are also infected. Our goal is to determine the extent to which detection of M. gallisepticum DNA or antibodies against the bacteria in a non-fringillid bird species is over- or underestimated using black-capped chickadees Poecile atricapillus, a species in which antibodies against M. gallisepticum are frequently detected in free-living individuals. After keeping black-capped chickadees in captivity for 12 weeks, during which period the birds remained negative for M. gallisepticum, four were inoculated with M. gallisepticum and four were sham inoculated in both eyes to serve as negative controls. Simultaneously we inoculated six house finches with the same isolate of M. gallisepticum as a positive control. All inoculated birds of both species developed infections detectable by qPCR in the conjunctiva. For the 6 weeks following inoculation we detected antibodies in all M. gallisepticum-inoculated house finches but in only three of the four M. gallisepticum-inoculated black-capped chickadees. All house finches developed severe eye lesions but none of the black-capped chickadees did. Modeling the Rapid Plate Agglutination test results of black-capped chickadees shows that the rate of false-positive tests would be not more than 3.2%, while the estimated rate of false negatives is 55%. We conclude that the proportion of wild-caught individuals in which we detect M. gallisepticum-specific antibodies using Rapid Plate Agglutination is, if anything, substantially underestimated.

Emergence of a new disease in a novel host is thought to be a rare outcome following frequent pathogen transfers between host species. However, few opportunities exist to examine whether disease emergence stems from a single successful pathogen transfer, and whether this successful lineage represents only one of several pathogen transfers between hosts. We examined the successful host transfer and subsequent evolution of the bacterial pathogen Mycoplasma gallisepticum, an emergent pathogen of house finches (Haemorhous (formerly Carpodacus) mexicanus). Our principal goals were to assess whether host transfer has been a repeated event between the original poultry hosts and house finches, whether only a single host transfer was ultimately responsible for the emergence of M. gallisepticum in these finches, and whether the spread of the pathogen from east to west across North America has resulted in spatial structuring in the pathogen. Using a phylogeny of M. gallisepticum based on 107 isolates from domestic poultry, house finches and other songbirds, we infer that the bacterium has repeatedly jumped between these two groups of hosts but with only a single lineage of M. gallisepticum persisting and evolving in house finches; bacterial evolution has produced monophyletic eastern and western North American subclades.

We performed experiments to test if American Goldfinches (Spinus tristis) could be a competent reservoir for Mycoplasma gallisepticum and play a role in the epidemic spread of mycoplasmal conjunctivitis among House Finches (Carpodacus mexicanus) in North America. We infected one of two individuals housed together in a cage and determined if transmission occurred to the second bird. Probability of transmission between an American Goldfinch and a House Finch (in either direction) was similar to that between two House Finches. In a second experiment small groups of birds (6-8) were housed in large aviaries. Two source birds were inoculated with M. gallisepticum, and transmission to the naive birds in the aviary was recorded. Transmission occurred among House Finches, among American Goldfinches, and from House Finches to American Goldfinches. Transmission was more likely between House Finches than among American Goldfinches, and between House Finches and American Goldfinches. We conclude that American Goldfinches are a competent reservoir for Mycoplasma gallisepticum and could have played a role in the spread of the epidemic as they are more migratory than House Finches.

The most effective approaches to control the spread of Mycoplasma gallisepticum include strict biosecurity measures, continuous surveillance and eradication of infected flocks. The rapid expansion of the poultry industry worldwide in restricted geographical areas and severe economic losses due to M. gallisepticum outbreaks make it crucial to identify and better control the vectors responsible for the transmission of the disease. In the present study we evaluated the susceptibility of sparrows and pigeons to M. gallisepticum and the tissue distribution of M. gallisepticum in these species as compared with chickens. This information will further define the role of these common avian species in M. gallisepticum transmission. Twenty-six chickens, pigeons, and sparrows were experimentally inoculated with a field strain of M. gallisepticum and were monitored for the development of clinical signs, seroconversion, productive infection by culture, and M. gallisepticum distribution in their tissues by immunohistochemistry. All M. gallisepticum-inoculated chickens showed mild respiratory signs, seroconverted (haemagglutination inhibition geometric mean titre = 494) and shed M. gallisepticum in their tracheas. M. gallisepticum antigens were observed at high levels by immunohistochemistry in their tracheas, conjunctivas, nasal turbinates, and air sacs. The pigeons and sparrows did not show clinical signs or seroconvert but M. gallisepticum was reisolated up to 7 days post inoculation from pigeons and intermittently from sparrows. M. gallisepticum antigens were observed at low level in the conjunctiva of some pigeons and sparrows, as well as in the trachea of some sparrows. We conclude that pigeons and sparrows are partially susceptible to M. gallisepticum infection but do not seroconvert or maintain a steady carrier state similar to chickens and that these species may play a role in M. gallisepticum transmission between poultry farms as mechanical vectors.

Host behaviour towards infectious conspecifics is a crucial yet overlooked component of pathogen dynamics. Selection is expected to favour individuals who can recognize and avoid infected conspecifics in order to reduce their own risk of infection. However, evidence is scarce and limited to species employing chemical cues. Here, we experimentally examine whether healthy captive house finches (Carpodacus mexicanus) preferentially forage near a same-sex, healthy conspecific versus one infected with the directly transmissible pathogen Mycoplasma gallisepticum (MG), which causes lethargy and visible conjunctivitis. Interestingly, male house finches strongly preferred feeding near diseased conspecifics, while females showed no preference. This sex difference appeared to be the result of lower aggression rates in diseased males, but not in females. The reduced aggression of diseased males may act as an 'evolutionary trap' by presenting a historically beneficial behavioural cue in the context of a new environment, which now includes a recently emerged, potentially fatal pathogen. Since MG can be directly transmitted during feeding, healthy males may inadvertently increase their risk of contracting MG. This behaviour is likely to significantly contribute to the continued persistence of MG epidemics in wild populations.

Mycoplasma gallisepticum 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. A key feature for the successful study of natural and experimental disease has been the apparent, very-high correlation between characteristic eye lesions and M. gallisepticum. Mycoplasma sturni was originally isolated from an adult European Starling (Sturnus vulgaris) with bilateral conjunctivitis and has since been reported in a relatively small number of other avian species, but not in House Finches. We identified as M. sturni a mycoplasma isolate from a California House Finch with conjunctivitis. However, experimental infection of House Finches with the M. sturni isolate failed to reproduce the disease. Therefore, M. gallisepticum remains the primary known cause of conjunctivitis in House Finches.

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.

The aim of this study was to evaluate the risk of transmission of Mycoplasma spp. from quarry to hunting falcons in the Middle East. Groups of 17 houbara bustards (Chlamydotis undulata) and 29 stone curlews (Burhinus oedicnemus) kept at three different private collections in Dubai were evaluated for the presence of Mycoplasma. Additionally, 10 falcons used for hunting were investigated for comparison. The falcons showed no clinical signs and were examined within the scope of a routine health check. From all birds, conjunctival and choanal swabs were taken and analyzed via polymerase chain reaction and culture. Although mycoplasmas were not recovered from choanal and conjunctival swabs taken from the houbara bustards, Mycoplasma gypis and M. falconis were isolated from the majority (28/29; 97%) of the stone curlews from choanal and conjunctival swabs. Most of the birds had no associated pathologic findings. Mycoplasma falconis was also detected in samples collected from 2 of the 10 falcons, and M. buteonis was isolated from the majority of falcons (6/10 falcons) from choanal (n = 5) and conjunctival (n = 1) swabs. Mycoplasma gypis could also be isolated from tissue samples (liver, oviduct, syrinx) of one dead stone curlew. This study presents the first isolation of mycoplasmas from stone curlews.

Mycoplasma gallisepticum has been isolated from various species of free-living birds, and we therefore tested the hypothesis that bird species other than the main host, the house finch (Carpodacus mexicanus), could play a role in the epidemiology of the infection. We compared the disease course in the house finch, American goldfinch (Carduelis tristis) and house sparrow (Passer domesticus) after inoculation into the conjunctival sac with M. gallisepticum, and also the degree to which the three species were infectious to other naive house finches. Severity of clinical signs was least in house sparrows, intermediate in American goldfinch and the highest in house finch. House sparrows were only mildly infectious to naive house finches for a short time, whereas American goldfinches remained infectious for up to 49 days post inoculation, although by then there were no physical signs of disease. We conclude that since American goldfinches can be infectious without showing any conjunctivitis, and since they often make long-distance movements, they might play an as yet unsuspected but important role in M. gallisepticum dynamics in house finches.

Mycoplasmas are well-known pathogens in a variety of animals. In poultry it is known that some species can be transmitted by semen and infect the uterus of females. As the prevalence of mycoplasmas in birds of prey is very high and artificial insemination is a commonly used technique for reproduction, the possibility of transmission Mycoplasma spp. by contaminated semen in birds of prey was investigated. Isolation of mycoplasmas was possible in five out of 32 (15.6%) semen samples of different bird of prey species. Two additional semen samples were positive for mycoplasma DNA using a Mycoplasma-genus-specific polymerase chain reaction. The isolation of mycoplasmas from a testicular sample indicates the testis as the possible source of contamination. Sequencing of large parts (>90%) of the 16S rRNA gene of the isolated mycoplasmas suggests that all isolates belong to the same species. Alignment of the sequenced products with the 16S rRNA gene of Mycoplasma species in GenBank demonstrated a similarity of 97% to Mycoplasma verecundum, but serological testing by immunobinding assay failed to identify it as such. It is recommended that the semen of donor birds of prey is examined for mycoplasmas before its use in artificial insemination.

Mycoplasmas are pathogens of different avian species, and they are able to be vertically transmitted. Even detected, Mycoplasma prevalence in raptor eggs is very low. In contrast to poultry, raptor eggs submitted for investigations are usually incubated. To investigate the influence of incubation length on the recovery of mycoplasmas from eggs, infertile specific-pathogen-free chicken eggs and embryos were infected with Mycoplasma lipofaciens (strain ML64), which had previously been isolated from an egg of a northern goshawk (Accipiter gentilis), in two different dosages. The eggs were investigated up to 12 days after infection (infertile eggs) or embryonic death. Mycoplasmas were recovered over the entire period after embryonic death by isolation. It was possible to re-isolate M. lipofaciens (strain ML64) from infertile eggs infected with 10(6) colony-forming units (CFUs) up to 12 days, but only up to 7 days if infected with 10(2) CFUs, which may be closer to the situation after natural infection. This study demonstrates that incubation of infertile eggs does have an influence on the recovery rate of mycoplasmas. This influence must be considered if interpreting results of Mycoplasma investigations in eggs of nonpoultry species. Additionally, it is recommended to use dead in shell embryos rather than infertile eggs for Mycoplasma detection.

The routes by which Mycoplasma gallisepticum initiates infection during outbreaks of conjunctivitis in house finches remain uncertain. As M. gallisepticum recovered from the cloaca of chickens remains viable for up to 3 days in chicken faeces, the possibility of spread via faecal contamination has been suggested. To test the hypothesis that food or water contaminated with M. gallisepticum may initiate infection, 20 house finches were experimentally inoculated by the oral or the conjunctival route. Clinical and immunological responses were compared. All inoculated birds seroconverted, thus demonstrating infection. Only two of the birds inoculated via the oral route developed very mild unilateral conjunctivitis while all 10 of those infected by eye-drop inoculation developed severe bilateral conjunctivitis. The orally inoculated birds had reduced levels of activity for only a few days, while those infected by conjunctival inoculation had reduced activity for several weeks. M. gallisepticum DNA was detected in conjunctival swabs by polymerase chain reaction in only three orally inoculated birds but in all birds in the conjunctivally inoculated group. Antibodies developed more slowly after oral inoculation than after conjunctival inoculation. We showed that oral exposure to M. gallisepticum can initiate infection, disease, and a serological response, which suggests that food or water contaminated with secretions or excretions may be a route of transmission between house finches.

Ever since Mycoplasma gallisepticum emerged among house finches in North America, it has been suggested that bird aggregations at feeders are an important cause of the epidemic of mycoplasmal conjunctivitis because diseased birds could deposit droplets of pathogen onto the feeders and thereby promote indirect transmission by fomites. In this paper we bring the first experimental evidence that such transmission (bird-to-feeder-to-bird) does actually take place. House finches infected via this route, however, developed only mild disease and recovered much more rapidly than birds infected from the same source birds but directly into the conjunctiva. While it is certainly probable that house finch aggregations at artificial feeders enhance pathogen transmission, to some degree transmission of M. gallisepticum by fomites may serve to immunize birds against developing more severe infections. Some such birds develop M. gallisepticum antibodies, providing indication of an immune response, although no direct evidence of protection.

In this paper we quantify the rate of spread of the newly emerged pathogen Mycoplasma gallisepticum of the House Finch, Carpodacus mexicanus, in its introduced range. We compare and contrast the rapid, yet decelerating, rate of spread of the pathogen with the slower, yet accelerating rate of spread of the introduced host. Comparing the rate of spread of this pathogen to pathogens in terrestrial mammalian hosts, we see that elevation and factors relating to host abundance restrict disease spread, rather than finding any major effects of discrete barriers or anthropogenic movement. We examine the role of seasonality in the rate of spread, finding that the rate and direction of disease spread relates more to seasonality in host movement than to seasonality in disease prevalence. We conclude that asymptomatic carriers are major transmitters of Mycoplasma gallisepticum into novel locations, a finding which may also be true for many other diseases, such as West Nile Virus and avian influenza.

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.

The use of controlled, horizontal-transmission experiments provides detailed information on the spread of disease within fixed social groups, which informs our understanding of disease dynamics both in an empirical and theoretical context. For that reason, we characterized in 2002, horizontal transmission of Mycoplasma gallisepticum (MG) in two flocks of 11 wild-caught house finches housed in outdoor aviaries over a 6-mo period. All birds were initially free of MG by a polymerase chain reaction (PCR)-based test, rapid plate agglutination (RPA), and the scoring of physical signs. We inoculated one flock member bilaterally in the palpebral conjunctiva and reintroduced it into its cage. Index birds developed conjunctivitis within 3 to 5 days but died 13 and 20 days postinfection (PI) possibly because of very severe weather. The proportion of birds with physical signs increased gradually, reached 40% at 6 wk PI, and fluctuated around 40% until 21 wk PI. By the time our experiment ended at 24.5 wk PI, 28% of the birds still exhibited physical signs. Across both flocks, 80% of the birds developed unilateral or bilateral conjunctivitis, and several birds relapsed. The appearance of physical signs in new individuals occurred between 10 and 144 days PI (median 41 days PI). Physical signs lasted 1-172 days (median 42 days). Birds that became infected earlier during the experiment developed more severe conjunctivitis, and there was a tendency for birds that developed bilateral conjunctivitis to develop physical signs earlier. Most birds that developed physical signs of MG were also PCR- and RPA-positive, although we detected a single asymptomatic carrier and a single symptomatic false negative. No birds died as a result of secondary MG infection.

Mycoplasmas have been implicated in certain clinical syndromes in ostriches and are associated with upper respiratory tract infections. As these infections result in production losses, they are of considerable economic importance to the South African ostrich industry. Although poultry mycoplasmas have been shown to infect ostriches, the existence of unique ostrich-specific mycoplasmas has been suggested. In this study, mycoplasmas were isolated from ostriches in the Klein Karoo, Central Karoo and Garden Route areas of the Western and Northern Cape Provinces of South Africa and identified using 16S rRNA gene sequencing. These sequences indicated that ostriches in these areas carry three unique mycoplasmas and were not infected with chicken mycoplasmas. Phylogenetic analysis of the 16S rRNA sequences of the three isolated ostrich mycoplasmas showed them to be quite divergent and to fall into two distinct phylogenetic groupings. Unique sequences within the 16S rRNA gene of the ostrich mycoplasmas were subsequently used for the development of specific primers for the detection and diagnosis of mycoplasma infections in ostriches. Chickens kept in close proximity to infected ostriches were not infected with these ostrich mycoplasmas.

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.

Long known as a pathogen of poultry, Mycoplasma gallisepticum (MG) was first detected in house finches in 1994. The disease rapidly spread throughout the eastern United States and Canada and was associated with debilitating disease and high mortality in house finches. However, in the late 1990s, the proportion of infected finches dying as a result of infection with MG decreased, and asymptomatic infection was more common among wild birds than in the past. We documented MG infections in breeding house finches and concluded that adults of both sexes transmit the infection to dependent young, probably after hatch. MG infections of breeding adults occurred late in the breeding season and were found in birds completing significantly more nests than birds that never tested positive for MG, implying that higher rates of reproduction carry a cost in the form of increased risk of infection. We found evidence of an MG-induced delay in dispersal of nestlings from their natal area and demonstrated a significant impact of infection on nestling growth.

Since 1994, an epidemic of conjunctivitis caused by Mycoplasma gallisepticum (MG) has spread throughout the eastern population of house finches (Carpodacus mexicanus). The adaptation of MG to a free-flying avian species presents potential problems for the control of mycoplasmosis in commercial poultry. To evaluate risks associated with this emerging problem, a field survey was conducted to assess prevalence of MG infection in house finches and other passerine birds associated with poultry farms. Between November 1997 and March 1999, 1058 birds were captured by mist net or trap at 17 farms and at 10 feeder stations in northeast Georgia. Birds were bled and screened by serum plate agglutination (SPA) for antibodies to MG. Birds with negative or weak positive SPA results were released at capture sites, and those with strong positive SPA reactions were kept for further evaluation. Necropsies were performed on selected house finches and individuals of 11 other passerine species, and samples were collected for MG testing by culture, polymerase chain reaction (PCR), hemagglutination inhibition, and histopathology. Testing revealed 19.1% of 671 birds caught at farms and 11.6% of 387 birds caught at feeder sites were SPA positive for MG. Three house finches captured on farms were positive for MG by culture and PCR, whereas three from feeder sites were positive only by PCR. No MG isolates were made from tufted titmice (Baeolophus bicolor), but 40% were positive by PCR. Individuals from 10 additional species were SPA positive only. Results suggest that MG persists at low levels in house finches in northeast Georgia and that tufted titmice may be nonclinical carriers of MG or a related mycoplasma. Positive SPA reactions in other species may be caused by nonspecific reactions or contact exposure. Current biosecurity recommendations should be sufficient to minimize risks of transmission between wild and domestic birds.

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.

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.

Although many new diseases have emerged within the past 2 decades [Cohen, M. L. (1998) Brit. Med. Bull. 54, 523-532], attributing low numbers of animal hosts to the existence of even a new pathogen is problematic. This is because very rarely does one have data on host abundance before and after the epizootic as well as detailed descriptions of pathogen prevalence [Dobson, A. P. & Hudson, P. J. (1985) in Ecology of Infectious Diseases in Natural Populations, eds. Grenfell, B. T. & Dobson, A. P. (Cambridge Univ. Press, Cambridge, U.K.), pp. 52-89]. Month by month we tracked the spread of the epizootic of an apparently novel strain of a widespread poultry pathogen, Mycoplasma gallisepticum, through a previously unknown host, the house finch, whose abundance has been monitored over past decades. Here we are able to demonstrate a causal relationship between high disease prevalence and declining house finch abundance throughout the eastern half of North America because the epizootic reached different parts of the house finch range at different times. Three years after the epizootic arrived, house finch abundance stabilized at similar levels, although house finch abundance had been high and stable in some areas but low and rapidly increasing in others. This result, not previously documented in wild populations, is as expected from theory if transmission of the disease was density dependent.

Although Mycoplasma gallisepticum (MG) is established in house finch (Carpodacus mexicanus) populations in at least 33 states, the potential risk of MG introduction to domestic poultry by infected finches currently is unknown. The objectives of this study were to determine if chickens could be infected with the finch strain of MG via direct, across-wire, and proximity (across-room) contact with naturally infected house finches and to determine if house finches could be infected through direct contact with experimentally infected chickens. Chickens were infected with the finch strain of MG through direct contact with naturally infected house finches, a determined by seroconversion (80%), polymerase chain reaction (PCR) (20%), and culture of MG (30%). Clinical disease was not observed in infected chickens. Isolates from chickens were identified as the original finch strain by arbitrary primed PCR. Transmission required an extended period of direct contact (10 wk) with infected finches, and no evidence of MG infection was detected in chickens exposed to infected finches across wire or across the room. Evidence of contact transmission of MG from infected chickens to house finches was limited to positive serum plate agglutination results, and infection could not be confirmed by PCR or culture. Results suggest that minimal biosecurity measures that restrict direct contact between chickens and house finches should significantly reduce the potential for MG transmission between these species.

A new mycoplasmal conjunctivitis was first reported in wild house finches (Carpodacus mexicanus) in early 1994. The causative agent was identified as Mycoplasma gallisepticum (MG), a nonzoonotic pathogen of poultry that had not been associated with disease in wild songbirds. Since the initial observations of affected house finches in the mid-Atlantic region, the disease has become widespread and has been reported throughout the eastern United States and Canada. By late 1995, mycoplasmal conjunctivitis had spread to an additional species, the American goldfinch (Carduelis tristis). This new disease exemplifies the rapid spread of a pathogen following introduction into a mobile wildlife population and provides lessons that may apply to emerging human diseases.

We inoculated game-farm mallard (Anas platyrhynchos) eggs and 1-day-old birds with Mycoplasma anatis to determine its effect on hatching success and growth rates of ducklings. Inoculations of eggs reduced hatching success, hatchling size, and duckling growth rates, compared to controls. Intratracheal inoculations of 1-day-old birds did not affect growth rates. Hatchlings and 1-day-old ducklings grew much slower for the first 7 to 10 days when raised at 17 to 19 C, compared to controls raised at 30 to 35 C. The effect of cold stress on growth was greater than the effect of M. anatis infection; we found no synergistic effects between cold stress and M. anatis infection.

House sparrows were infected by aerosol with Mycoplasma gallisepticum (MG) or M. synoviae (MS). MG was reisolated from 5 to 11 sparrows 10 days postinfection, but infection appeared to be temporary. Mycoplasma-free chickens reared in the experimental house became infected with MG during the trial. MS was recovered from only one sparrow. Serological tests were unsatisfactory for diagnosing infected birds. The results suggest that house sparrows may be temporary biological carriers of MG.