Conjunctivitis In House Finches Research Articles

Disease tolerance alters host competence in a wild songbird.

Individuals can express a range of disease phenotypes during infection, with important implications for epidemics. Tolerance, in particular, is a host response that minimizes the per-pathogen fitness costs of infection. Because tolerant hosts show milder clinical signs and higher survival, despite similar pathogen burdens, their potential for prolonged pathogen shedding may facilitate the spread of pathogens. To test this, we simulated outbreaks of mycoplasmal conjunctivitis in house finches, asking how the speed of transmission varied with tissue-specific and behavioural components of tolerance, milder conjunctivitis and anorexia for a given pathogen load, respectively. Because tissue-specific tolerance hinders pathogen deposition onto bird feeders, important transmission hubs, we predicted it would slow transmission. Because behavioural tolerance should increase interactions with bird feeders, we predicted it would speed transmission. Our findings supported these predictions, suggesting that variation in tolerance could help identify individuals most likely to transmit pathogens.

Apparent effect of chronic Plasmodium infections on disease severity caused by experimental infections with Mycoplasma gallisepticum in house finches.

An epidemic caused by a successful host jump of the bacterial pathogen Mycoplasma gallisepticum from poultry to house finches in the 1990s has by now spread across most of North America. M. gallisepticum causes severe conjunctivitis in house finches. We experimentally show that M. gallisepticum transmission to birds with or without chronic Plasmodium infection does not differ. However, once infected with M. gallisepticum house finches chronically infected with Plasmodium develop more severe clinical disease than birds without such infection. We speculate as to possible effects of coinfection.

House Finch (Haemorhous mexicanus) Conjunctivitis, and Mycoplasma spp. Isolated from North American Wild Birds, 1994-2015.

Sampling wild birds for mycoplasma culture has been key to the study of House Finch (Haemorhous mexicanus) conjunctivitis, yielding isolates of Mycoplasma gallisepticum spanning the temporal and geographic ranges of disease from emergence to endemicity. Faced with the challenges and costs of sample collection over time and from remote locations for submission to our laboratory for mycoplasma culture, protocols evolved to achieve a practical optimum. Herein we report making M. gallisepticum isolates from House Finches almost every year since the disease emerged in 1994, and we now have 227 isolates from 17 states. Our wild bird host range for M. gallisepticum isolates includes Blue Jay ( Cyanocitta cristata ), American Goldfinch (Spinus tristis), Lesser Goldfinch (Spinus psaltria), Purple Finch (Haemorhous purpureus), Evening Grosbeak ( Coccothraustes vespertinus ), and herein first reports for Western Scrub-jay ( Aphelocoma californica ), and American Crow ( Corvus brachyrhynchos ). By collecting and identifying isolates from birds with clinical signs similar to those of House Finch conjunctivitis, we also expanded the known host range of Mycoplasma sturni and obtained isolates from additional wild bird species. Accumulating evidence shows that a diverse range of wild bird species may carry or have been exposed to M. gallisepticum in the US, as in Europe and Asia. Therefore, the emergence of a pathogenic M. gallisepticum strain in House Finches may actually be the exception that has allowed us to identify the broader epidemiologic picture.

Deposition of pathogenic Mycoplasma gallisepticum onto bird feeders: host pathology is more important than temperature-driven increases in food intake

Although ambient temperature has diverse effects on disease dynamics, few studies have examined how temperature alters pathogen transmission by changing host physiology or behaviour. Here, we test whether reducing ambient temperature alters host foraging, pathology and the potential for fomite transmission of the bacterial pathogen Mycoplasma gallisepticum (MG), which causes seasonal outbreaks of severe conjunctivitis in house finches (Haemorhous mexicanus). We housed finches at temperatures within or below the thermoneutral zone to manipulate food intake by altering energetic requirements of thermoregulation. We predicted that pathogen deposition on bird feeders would increase with temperature-driven increases in food intake and with conjunctival pathology. As expected, housing birds below the thermoneutral zone increased food consumption. Despite this difference, pathogen deposition on feeders did not vary across temperature treatments. However, pathogen deposition increased with conjunctival pathology, independently of temperature and pathogen load, suggesting that MG could enhance its transmission by increasing virulence. Our results suggest that in this system, host physiological responses are more important for transmission potential than temperature-dependent alterations in feeding. Understanding such behavioural and physiological contributions to disease transmission is critical to linking individual responses to climate with population-level disease dynamics.

Mycoplasmosis in wildlife: a review

Mycoplasma, the smallest self-replicating life-forms, are responsible for a variety of diseases in humans, domestic animals, insects, and plants. Although the exact role of these organisms in wildlife is not available, now it is increasingly recognized that mycoplasmosis is an emerging disease in many wildlife populations. As only scattered data regarding these are available, an attempt has been made to assemble the available literature. To our knowledge, this is the first review paper regarding mycoplasmosis in wildlife. The outbreaks of mycoplasmoses such as contagious pleuropneumonia (CCPP), infectious keratoconjunctivitis (IKC), Mycoplasma ovipneumoniae and Mycoplasma capricolum subspp. capricolum infections, and contagious agalactia in wild ruminants; mycoplasmosis in raccoons; upper respiratory tract disease (URTD) and Mycoplasma crocodyli and Mycoplasma alligatoris infections in wild reptiles; and house finch conjunctivitis are showing that the prevalence of mycoplasmosis in wildlife has reached an alarming level, thus raising concerns for the conservation of many endangered species in captivity and free-ranging populations. These also emphasize the urgent need for increased surveillance and control of mycoplasma in wildlife. Some control approaches that can be followed are prevention of the spillover from domestic livestock and birds, proper quarantine of newly received animals along with mycoplasma screening, isolation of affected and suspected animals, screening of mycoplasmoses before the release of captive animals into free-ranging population, etc. At the same time, the previous dogma that mycoplasma have strict host specificity should be reconsidered in the light of new findings.

Do infections lead to higher feather mite loads in birds? A test with mycoplasmal conjunctivitis in House Finches (Haemorhous mexicanus)

Abstract. Current evidence suggests that the health effect of avian feather mites is minimal. However, feather mites can still proliferate without effective preening, such as might occur during sickness. House Finches (Haemorhous mexicanus) are prone to infection by Mycoplasma gallisepticum, symptoms of which include conjunctivitis. Impaired vision and lethargy associated with the disease may limit preening ability. We examined trapping data from a 4-year study of Mycoplasma infection dynamics in House Finches in Atlanta, Georgia, to determine whether birds with conjunctivitis had higher feather mite loads. Abundance of feather mites (Proctophyllodes spp.) and conjunctivitis severity were visually scored on >800 House Finches of known age and sex. Feather mite abundance showed a distinct seasonal pattern: mite loads increased in July and remained high through January. Limiting the analyses to these months, we found that average mite scores were higher in birds with (n = 94) than in those without (n = 275)...

Chronic Mycoplasma conjunctivitis in house finches: Host antibody response and M. gallisepticum VlhA expression

Previous studies have shown that house finch field isolates of Mycoplasma gallisepticum (MG) vary in virulence and ability to induce an antibody response. After experimental inoculation, MG causes persistent, severe disease in a subset of individuals. In this study, we further characterized MG infection using five field isolates, with an emphasis on chronically diseased birds. After experimental inoculation of house finches, MG load was measured by quantitative PCR and anti-MG antibody responses were measured by ELISAs. Birds with chronic disease had significantly higher pathogen loads and antibody responses than did birds without chronic disease. Using a monoclonal antibody (MAb86) specific for a variant of the MG VlhA adhesin and immunodominant surface protein, we show that VlhA expression differs among MG isolates in this study, and that in vivo VlhA changes occur in house finches infected with MG. Overall, our results suggest that chronic MG disease has a strong pathogen-mediated component.

Mycoplasmal Conjunctivitis in House Finches (Carpodacus Mexicanus) is More Severe in Left Eyes than Right

One of the most well-studied avian diseases is the annual outbreak of Mycoplasma gallisepticum (MG) infections in house finches (Carpodacus mexicanus) in North America. This is a bacterial disease that causes conjunctivitis in one or both eyes of the host. While studying this disease in a New York finch population, researchers observed that there was a tendency for the conjunctivitis to be more prominent in the left eye of infected birds, although the small sample size of that study made it difficult to draw conclusions regarding this unusual observation. Here, this idea is tested further using a larger data set from a 4-year trapping study of house finches in Atlanta, Georgia, USA, a location with a high prevalence of MG infections. The severity of conjunctivitis in each eye of infected birds was scored on a 0–3 scale, and these data were statistically examined to identify possible side-biases in severity. Out of 254 house finches with conjunctivitis, the eye scores of all left eyes were significantly higher than right eye scores. There was no evidence for differential effects of conjunctivitis in left-bias or right-biased infections, and the left-biased pattern was similar in both sexes and in adult and young birds. These results confirm the anecdotal observation from the New York population and suggest that this is a universal phenomenon in the house finch–MG system. The significance of the finding is unknown, although the possibility exists that house finches display a degree of ‘handedness’ that causes their left sides to be exposed more frequently to potential fomites (i.e. bird feeders).

Mycoplasma sturni from a California House Finch with Conjunctivitis Did Not Cause Disease in Experimentally Infected House Finches

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.

Effects of route of inoculation on Mycoplasma gallisepticum infection in captive house finches

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.

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.

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.

Dynamics of a novel pathogen in an avian host: Mycoplasmal conjunctivitis in house finches

In early 1994, a novel strain of Mycoplasma gallisepticum (MG)—a poultry pathogen with a world-wide distribution—emerged in wild house finches and within 3 years had reached epidemic proportions across their eastern North American range. The ensuing epizootic resulted in a rapid decline of the host population coupled with considerable seasonal fluctuations in prevalence. To understand the dynamics of this disease system, a multi-disciplinary team composed of biologists, veterinarians, microbiologists and mathematical modelers set forth to determine factors driving and influenced by this host–pathogen system. On a broad geographic scale, volunteer observers (“citizen scientists”) collected and reported data used for calculating both host abundance and disease prevalence. The scale at which this monitoring initiative was conducted is unprecedented and it has been an invaluable source of data for researchers at the Cornell Laboratory of Ornithology to track the spread and magnitude of disease both spatially and temporally. At a finer scale, localized and intensive field studies provided data used to quantify the effects of disease on host demographic parameters via capture–mark–recapture modeling, effects of host behavior on disease and vice-versa, and the biological and genetic profiles of birds with known phenotypic characteristics. To balance the field-based component of the study, experiments were conducted with finches held in captivity to describe and quantify the effects of experimental infections on hosts in both individual and social settings. The confluence of these various elements of the investigation provided the foundation for construction of a general compartmentalized epidemiological model of the dynamics of the house finch–MG system. This paper serves several purposes including (i) a basic review of the pathogen, host, and epidemic cycle; (ii) an explanation of our research strategy; (iii) a basic review of results from the diverse multi-disciplinary approaches employed; and (iv) pertinent questions relevant to this and other wildlife disease studies that require further investigation.

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.

New and Re-Emerging Infectious Diseases

The seventh annual Conference on New and Re-Emerging Infectious Diseases, April 15–16, 2004, was hosted by the Center for Zoonoses Research and the College of Veterinary Medicine at the University of Illinois at Urbana-Champaign. The conference featured eight speakers and 31 poster presentations. The conference was opened with a presentation on Yersinia enterocolitica, a gram-negative enteric human pathogen that causes enterocolitis. Invasin is the primary requirement for efficient translocation of the bacteria across the intestinal epithelium; the identification of both positive and negative regulators of its expression have been identified. The emergence of Mycoplasma gallisepticum, which causes severe conjunctivitis in house finches, was described. The strain of M. gallisepticum that affects house finches, a new host recently introduced to North America, is a novel strain that emerged recently. Current therapies for microsporidiosis, a serious opportunistic infection in persons with AIDS, organ transplant recipients, children, travelers, contact lens wearers, and the elderly, were reviewed. Studies on the human fungal pathogen Cryptococcus neoformans, which causes life-threatening infections of the central nervous system, most commonly in immunocompromised hosts, were reported. The studies focused on signaling cascades that govern virulence and an unusual mating type locus linked to differentiation and virulence. It was shown that release of the variant surface antigens of African trypanosomes, agents of a reemerging infectious disease in sub-Saharan Africa, occurs not only by proteolysis but also by glycosylphosphatidylinositol-anchor hydrolysis through a phospholipase present in the parasite surface. To characterize the human colonic response to Shigella and Entamoeba histolytica at the molecular level, differential transcription of nearly 40,000 human genes in sections of human colonic xenografts that had been infected with Shigella flexneri or E. histolytica was measured. The results indicated increased expression of genes encoding proteins involved in stress, hypoxic responses, immune and inflammatory responses, responses to tissue injury and tissue repair, cytokines, and chemokines. Studies on sortases, membrane-anchored transpeptidases that cleave surface proteins, were described. Because sortases of Staphylococcus aureus are required for animal infections, inhibitors that disrupt the activity of sortases may be therapeutically useful. The conference was concluded with a description of the severe acute respiratory syndrome (SARS) epidemic in China. China's handling of the epidemic has been critiqued by the international community, but a balanced view of events has shown that many measures undertaken by officials, such as large-scale quarantines, mandatory fever-screening checkpoints, arrival and departure monitoring at airports, populationwide surveillance, community infection control, and designating SARS-only hospitals, worked effectively to contain this infectious disease. The proceedings are available in PDF format at http://www.cvm.uiuc.edu/czr/

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.

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.

Risk factors associated with mycoplasmal conjunctivitis in house finches.

Observations from a citizen-based survey were used to identify potential risk factors associated with mycoplasmal conjunctivitis (Mycoplasma gallisepticum) in eastern house finches (Carpodacus mexicanus). Between November 1994 and October 1996, 778 volunteers provided 7,224 monthly observations at residential bird feeding sites across an eight state region in the eastern USA. Information collected by questionnaires included health status of house finches and four sympatric passerine species, types and number of bird feeders maintained, neighborhood housing locale and altitude of the observation site. Bivariate analyses revealed that house finches were 14 to 72 times as likely to be observed with conjunctivitis than the sympatric species studied. Year of the study, season, and the presence of platform, hopper, and tube type feeders were significantly associated with conjunctivitis in house finches. Multivariate analysis using a logistic regression model suggests that increased risk of conjunctivitis in house finches was associated with the second year of the study (the third year of the outbreak), the cooler non-breeding periods from September through March, and the presence of tube style feeders. In addition, the presence of raised platform type feeders may have been protective against conjunctivitis in house finches. Prevention of spread of this disease may include modifying bird feeding activities based on season and type of feeder.

Mycoplasma sturni from blue jays and northern mockingbirds with conjunctivitis in Florida.

Northern mockingbirds (Mimus polyglottos) and blue jays (Cyanocitta cristata) in a Florida (USA) wildlife care facility developed clinical signs and gross lesions suggestive of the ongoing outbreak of Mycoplasma gallisepticum (MG) conjunctivitis in house finches (Carpodacus mexicanus) and American goldfinches (Carduelis tristis). Mycoplasmal organisms were cultured from conjunctival/corneal swabs of birds with sinusitis, conjunctivitis, and/or epiphora. All of the isolates tested were identified as Mycoplasma sturni by indirect immunofluorescence. Mycoplasma sturni as well as MG should be considered in the differential diagnosis of songbirds with conjunctivitis.

Natural Mycoplasma gallisepticum infection in a captive flock of house finches.

Naturally-occurring mycoplasmal conjunctivitis is described among 104 wild-caught, and initially seronegative, house finches (Carpodacus mexicanus) maintained in captivity for 12 wk during November 1995 through January 1996. Finches housed in three pens were monitored for clinical signs, and > or = 10 birds were euthanatized for necropsy and mycoplasma testing every 2 wk. Within 2 to 4 wk following initial detection of lesions, > 50% of the birds in each of three pens developed a debilitating disease characterized by mild to severe ocular swelling, conjunctivitis, and ocular and nasal discharge. Microscopic lesions in affected finches consisted of mild to severe lymphoplasmacytic inflammation with epithelial and lymphoid hyperplasia in conjunctivae, nasal turbinates, and trachea. Mycoplasma gallisepticum infection was confirmed by culture or polymerase chain reaction (PCR) in all birds with conjunctival lesions and in 43% of birds without lesions. An arbitrary primer PCR was used to confirm M. gallisepticum isolates as identical to a field strain previously associated with house finch conjunctivitis. Most birds (89%) with conjunctivitis developed a concurrent antibody response detectable by serum plate agglutination (SPA) within 2 wk of lesion development. Hemagglutination inhibition (HI) and enzyme-linked immunosorbent assay (ELISA) tests were less sensitive than the SPA test. The clinical severity of this disease and high proportion of affected birds suggests that M. gallisepticum may have a negative impact on free-flying house finch populations.