Pathology of experimental Sarcocystis falcatula infections of canaries (Serinus canarius) and pigeons (Columba livia)

Sarcocystis falcatula is an apicomplexan parasite with a broad range of avian intermediate hosts. The pathology and pathogenesis of infection with this parasite has been studied experimentally in the budgerigar (Melopsittacus undulatus). The present study quantitatively examines the pathology of this parasite in canaries (Serinus canarius) and pigeons (Columba livia) and compares it with that found in budgerigars. The general progression of merogony and cyst formation is similar qualitatively to that seen in budgerigars, but it differs quantitatively. The principal site of precystic merogony is in pulmonary endothelial cells. The magnitude of pulmonary meront burdens (at similar inoculated dosages) varies in different intermediate host species. Merogony is less persistent than in budgerigars. Among the various species of birds, the magnitude of precystic merogony correlates differently with the magnitude of skeletal muscle cyst burdens. The distribution of cyst burdens among various muscles also differs. The composition of inflammatory cells differs among various avian species' response to S. falcatula. Pathologic changes quantitatively parallel tissue meront burdens (except possibly in the liver of canaries), resulting in an interstitial pneumonitis, hepatitis, and mild inflammatory lesions of other organs.     

Description of Sarcocystis falcatula Stiles, 1893, a Parasite of Birds and Opossums1

ABSTRACT. Sarcocystis falcatula Stiles, 1893 is re-described. Intermediate hosts of the parasite which was earlier described as Sarcocystis debonei Vogelsang, 1929 are species of passeriform, psittaciform, and columbiform birds. In these birds, muscle zoites are 6.88 × 2.19 (4.8-8.4 × 1.2-3.6) μm and are enclosed in a cyst wall with regular protrusions, 1-5 μm long. The convoluted primary wall has multiple thin areas in the osmiophilic layer. Microtubules originate in the ground substance and extend to the tips of the protrusions. The only known definitive host is the opossum, Didelphis virginiana; rats, cats, a dog, and a ferret could not be infected from muscle cysts. Sporocysts from opossums infected from five different infected avian sources measure 11.2 × 7.4 (9.6?12.0 × 6.0-8.4)μm.     

Plasmodium relictum (lineage P-SGS1): effects on experimentally infected passerine birds

We evaluated the effects of Plasmodium relictum (lineage P-SGS1), which is a host generalist, to five species of passerine birds. Light infection of P. relictum was isolated from a naturally infected adult reed warbler Acrocephalus scirpaceus. The parasites were inoculated to naive juveniles of the chaffinch Fringilla coelebs, common crossbill Loxia curvirostra, house sparrow Passer domesticus, siskin Spinus spinus and starling Sturnus vulgaris. Susceptibility of these birds to the infection of P. relictum was markedly different. This parasite developed in birds belonging to the Fringillidae and Passeridae but the starlings (Sturnidae) were resistant. Only 50% of experimental house sparrows were susceptible to the infection. The intensity of parasitemia varied markedly inside and between different susceptible bird species. There were no effects of the infection on body mass or temperature of experimentally infected birds. Infection of P. relictum leads to the significant decrease of haematocrit value and hypertrophy of spleen and liver in heavily infected common crossbills and siskins. This study shows that infection of the same lineage of P. relictum causes diseases of different severity in different avian hosts; that might have different evolutionary consequences and should be taken in consideration in conservation projects.     

Experimental transmission of Sarcocystis from icterid birds to sparrows and canaries by sporocysts from the opossum.

Cowbirds (Molothrus ater) and grackles (Cassidix mexicanus) infected with muscle cysts of Sarcocystis were fed to opposums (Didelphis virginiana) and fecal sporocysts from the latter were given to sparrows (Passer domesticus, Family Ploceidae), canaries (Serinus canarius, Family Fringillidae) and ducks (Anas platyrhynchos, Family Anatidae). Asexual parasites were found in the endothelium of sparrows and canaries but not in ducks. When birds were kept 10 weeks or more after infection, muscle cysts were found grossly and microscopically in the majority of sparrows, and in 1 canary, but not in ducks. Muscle zoites were found in digests of all sparrows and canaries but not in that of ducks. Metrocytes and forms dividing by endodyogeny also were found in the digest. Thus, avian Sarcocystis was transmitted experimentally from 2 genera of 1 family (Icteridae) to 2 different families of passerine intermediate hosts by sporocysts from the definitive host. This is the broadest intermediate host spectrum known for a species of Sarcocystis.     

Plasmodium relictum (lineage SGS1) and Plasmodium ashfordi (lineage GRW2): the effects of the co-infection on experimentally infected passerine birds

The effects of avian malaria parasites of the genus Plasmodium on their hosts are insufficiently understood. This is particularly true for malarial co-infections, which predominant in many bird populations. We investigated effects of primary co-infection of Plasmodium relictum (lineage SGS1) and Plasmodium ashfordi (GRW2) on experimentally infected naive juveniles of siskin Spinus spinus, crossbill Loxia curvirostra and starling Sturnus vulgaris. All siskins and crossbills were susceptible but starlings resistant to both these infections. A general pattern of the co-infections was that heavy parasitemia (over 35% during peaks) of both parasites developed in both susceptible host species. There were no significant effects of the co-infections on mean body mass of the majority of infected birds. Mean haematocrit value decreased approximately 1.5 and 3 times in siskins and crossbills at the peak of parasitemia, respectively. Mortality was recorded among infected crossbills. We conclude that co-infections of P. relictum and P. ashfordi are highly virulent and act synergetically during primary infections in some but not all passerine birds.     

Lack of Sarcocystis neurona antibody response in Virginia opossums (Didelphis virginiana) fed Sarcocystis neurona-infected muscle tissue

Serum was collected from laboratory-reared Virginia opossums (Didelphis virginiana) to determine whether experimentally infected opossums shedding Sarcocystis neurona sporocysts develop serum antibodies to S. neurona merozoite antigens. Three opossums were fed muscles from nine-banded armadillos (Dasypus novemcinctus), and 5 were fed muscles from striped skunks (Mephitis mephitis). Serum was also collected from 26 automobile-killed opossums to determine whether antibodies to S. neurona were present in these opossums. Serum was analyzed using the S. neurona direct agglutination test (SAT). The SAT was modified for use with a filter paper collection system. Antibodies to S. neurona were not detected in any of the serum samples from opossums, indicating that infection in the opossum is localized in the small intestine. Antibodies to S. neurona were detected in filter-paper-processed serum samples from 2 armadillos naturally infected with S. neurona.     

Susceptibility of wood ducks to H5N1 highly pathogenic avian influenza virus

Since 2002, H5N1 highly pathogenic avian influenza (HPAI) viruses have caused mortality in numerous species of wild birds; this is atypical for avian influenza virus (AIV) infections in these avian species, especially for species within the order Anseriformes. Although these infections document the susceptibility of wild birds to H5N1 HPAI viruses and the spillover of these viruses from infected domestic birds to wild birds, it is unknown whether H5N1 HPAI viruses can persist in free-living avian populations. In a previous study, we established that wood ducks (Aix sponsa) are highly susceptible to infection with H5N1 HPAI viruses. To quantify this susceptibility and further evaluate the likelihood of H5N1 HPAI viral maintenance in a wild bird population, we determined the concentration of virus required to produce infection in wood ducks. To accomplish this, 25 wood ducks were inoculated intranasally at 12-16 wk of age with decreasing concentrations of a H5N1 HPAI virus (A/Whooper Swan/Mongolia/244/05 [H5N1]). The median infectious dose and the lethal dose of H5N1 HPAI virus in wood ducks were very low (10(0.95) and 10(1.71) median embryo infectious dose [EID(50)]/ml, respectively) and less than that of chickens (10(2.80) and 10(2.80) EID(50)/ml). These results confirm that wood ducks are highly susceptible to infection with H5N1 HPAI virus. The data from this study, combined with what is known experimentally about H5N1 HPAI virus infection in wood ducks and viral persistence in aquatic environments, suggest that the wood duck would represent a sensitive indicator species for H5N1 HPAI. Results also suggest that the potential for decreased transmission efficiency associated with reduced viral shedding (especially from the cloaca) and a loss of environmental fitness (in water), may be offset by the ability of this virus to be transmitted through a very low infectious dose.     

Experimental studies of St. Louis encephalitis virus in vertebrates

Serologically negative birds and mammals of species, known from other studies to be exposed naturally to St. Louis encephalitis (SLE) virus in Memphis, Tennessee, and other selected species were inoculated experimentally with strains of SLE virus to determine their potential as natural hosts. Mosquitoes (Culex sp.) were allowed to feed on some of the inoculated vertebrate species, held for 14 days, and tested for SLE infection. The cardinals (Richmondena cardinalis), robins (Turdus migratorius), and baby chicks (Gallus gallus) all became viremic; 97% of the bobwhites (Colinus virginianus) and 20% of the Japanese quail (Coturnix coturnix) became viremic. No viremia was detected in raccoons (Procyon lotor), opossums (Didelphis virginiana), or adult cotton rats (Sigmodon hispidus). Only 20% of cottontail rabbits (Sylvilagus audubonii), 50% of wood rats (Neotoma mexicana), and 75% of hamsters (Mesocricetus auratus) but all the young cotton rats and least chipmunks (Eutamias minimus) were susceptible. Robins had the highest titered viremia but were viremic for the shortest period of time. Bobwhites had lower peak viremia titers but for a longer duration. Biologic differences in the response of some vertebrates to different SLE strains were noted. Culex pipiens quinquefasciatus mosquitoes readily became infected after feeding on viremic cardinals. Comparisons of the experimental data with information obtained from field investigations provided a better understanding of the contributions of the various vertebrate species to the transmission and maintenance of SLE virus in nature.     

Novel Pathways Revealed in Bursa of Fabricius Transcriptome in Response to Extraintestinal Pathogenic Escherichia coli (ExPEC) Infection

Extraintestinal pathogenic Escherichia coli (ExPEC) has major negative impacts on human and animal health. Recent research suggests food-borne links between human and animal ExPEC diseases with particular concern for poultry contaminated with avian pathogenic E. coli (APEC), the avian ExPEC. APEC is also a very important animal pathogen, causing colibacillosis, one of the world’s most widespread bacterial diseases of poultry. Previous studies showed marked atrophy and lymphocytes depletion in the bursa during APEC infection. Thus, a more comprehensive understanding of the avian bursa response to APEC infection will facilitate genetic selection for disease resistance. Four-week-old commercial male broiler chickens were infected with APEC O1 or given saline as a control. Bursas were collected at 1 and 5 days post-infection (dpi). Based on lesion scores of liver, pericardium and air sacs, infected birds were classified as having mild or severe pathology, representing resistant and susceptible phenotypes, respectively. Twenty-two individual bursa RNA libraries were sequenced, each yielding an average of 27 million single-end, 100-bp reads. There were 2469 novel genes in the total of 16,603 detected. Large numbers of significantly differentially expressed (DE) genes were detected when comparing susceptible and resistant birds at 5 dpi, susceptible and non-infected birds at 5 dpi, and susceptible birds at 5 dpi and 1 dpi. The DE genes were associated with signal transduction, the immune response, cell growth and cell death pathways. These data provide considerable insight into potential mechanisms of resistance to ExPEC infection, thus paving the way to develop strategies for ExPEC prevention and treatment, as well as enhancing innate resistance by genetic selection in animals.     

A survey of avian influenza in tree sparrows in China in 2011

Tree sparrows (Passer montanus) are widely distributed in all seasons in many countries. In this study, a survey and relevant experiments on avian influenza (AI) in tree sparrows were conducted. The results suggested that the receptor for avian influenza viruses (AIVs), SAα2,3Gal, is abundant in the respiratory tract of tree sparrows, and most of the tree sparrows infected experimentally with two H5 subtype highly pathogenic avian influenza (HPAI) viruses died within five days after inoculation. Furthermore, no AIVs were isolated from the rectum eluate of 1300 tree sparrows, but 94 serological positives of AI were found in 800 tree sparrows. The serological positives were more prevalent for H5 subtype HPAI (94/800) than for H7 subtype AI (0/800), more prevalent for clade 2.3.2.1 H5 subtype HPAI (89/800) than for clade 2.3.4 (1/800) and clade 7.2 (4/800) H5 subtype HPAI, more prevalent for clade 2.3.2.1 H5 subtype HPAI in a city in southern China (82/800) than in a city in northern China (8/800). The serological data are all consistent with the distribution of the subtypes or clades of AI in poultry in China. Previously, sparrows or other passerine birds were often found to be pathogenically negative for AIVs, except when an AIV was circulating in the local poultry, or the tested passerine birds were from a region near waterfowl-rich bodies of water. Taken together, the data suggest that tree sparrows are susceptible to infection of AIVs, and surveys targeting sparrows can provide good serological data about the circulation of AIVs in relevant regions.     

Implications of raccoon latrines in the epizootiology of baylisascariasis.

Raccoons (Procyon lotor) frequently establish defecation sites, termed latrines, on large logs, stumps, rocks, and other horizontally oriented structures/surfaces. These latrines are important foci of infective eggs of Baylisascaris procyonis, a nematode parasite of raccoons which is pathogenic to numerous species of mammals and birds. To examine the role of raccoon latrines in this animal-parasite interaction, we documented animal visitations to raccoon latrines in two large forested tracts and two woodlots in Indiana (USA) during 1994 and 1995. Species richness of vertebrate visitors did not differ between sites or years, but species composition differed by site and year. Fourteen mammal and 15 bird species were documented visiting raccoon latrines. Small granivorous mammals, including white-footed mice (Peromyscus leucopus), eastern chipmunks (Tamias striatus), and tree squirrels (Sciurus carolinensis, S. niger, Tamiasciurus hudsonicus) were the most common visitors to latrine sites. White-footed mice, chipmunks, white-breasted nuthatches (Sitta carolinensis), and opossums (Didelphis virginiana) were photographed foraging on undigested seeds in raccoon feces. Active foraging at latrines also was shown experimentally; seeds embedded in raccoon feces were removed at a greater rate at latrine sites than at nonlatrines. We conclude that raccoon latrines are visited routinely by a variety of vertebrates, especially small granivorous rodents and birds which forage for seeds in raccoon feces, and that raccoon latrines are probable sites of transmission of B. procyonis to susceptible mammals and birds.     

Experimental Evidence for Evolved Tolerance to Avian Malaria in a Wild Population of Low Elevation Hawai‘i ‘Amakihi (Hemignathus virens)

Introduced vector-borne diseases, particularly avian malaria (Plasmodium relictum) and avian pox virus (Avipoxvirus spp.), continue to play significant roles in the decline and extinction of native forest birds in the Hawaiian Islands. Hawaiian honeycreepers are particularly susceptible to avian malaria and have survived into this century largely because of persistence of high elevation refugia on Kaua‘i, Maui, and Hawai‘i Islands, where transmission is limited by cool temperatures. The long term stability of these refugia is increasingly threatened by warming trends associated with global climate change. Since cost effective and practical methods of vector control in many of these remote, rugged areas are lacking, adaptation through processes of natural selection may be the best long-term hope for recovery of many of these species. We document emergence of tolerance rather than resistance to avian malaria in a recent, rapidly expanding low elevation population of Hawai‘i ‘Amakihi (Hemignathus virens) on the island of Hawai‘i. Experimentally infected low elevation birds had lower mortality, lower reticulocyte counts during recovery from acute infection, lower weight loss, and no declines in food consumption relative to experimentally infected high elevation Hawai‘i ‘Amakihi in spite of similar intensities of infection. Emergence of this population provides an exceptional opportunity for determining physiological mechanisms and genetic markers associated with malaria tolerance that can be used to evaluate whether other, more threatened species have the capacity to adapt to this disease.     

Demographic and Spatiotemporal Patterns of Avian Influenza Infection at the Continental Scale,and in Relation to Annual Life Cycle of a Migratory Host

Since the spread of highly pathogenic avian influenza (HPAI) H5N1 in the eastern hemisphere, numerous surveillance programs and studies have been undertaken to detect the occurrence, distribution, or spread of avian influenza viruses (AIV) in wild bird populations worldwide. To identify demographic determinants and spatiotemporal patterns of AIV infection in long distance migratory waterfowl in North America, we fitted generalized linear models with binominal distribution to analyze results from 13,574 blue-winged teal (Anas discors, BWTE) sampled in 2007 to 2010 year round during AIV surveillance programs in Canada and the United States. Our analyses revealed that during late summer staging (July-August) and fall migration (September-October), hatch year (HY) birds were more likely to be infected than after hatch year (AHY) birds, however there was no difference between age categories for the remainder of the year (winter, spring migration, and breeding period), likely due to maturing immune systems and newly acquired immunity of HY birds. Probability of infection increased non-linearly with latitude, and was highest in late summer prior to fall migration when densities of birds and the proportion of susceptible HY birds in the population are highest. Birds in the Central and Mississippi flyways were more likely to be infected compared to those in the Atlantic flyway. Seasonal cycles and spatial variation of AIV infection were largely driven by the dynamics of AIV infection in HY birds, which had more prominent cycles and spatial variation in infection compared to AHY birds. Our results demonstrate demographic as well as seasonal, latitudinal and flyway trends across Canada and the US, while illustrating the importance of migratory host life cycle and age in driving cyclical patterns of prevalence.     

Antibodies against Pasteurella multocida in snow geese in the western Arctic.

To determine if lesser snow geese (Chen caerulescens caerulescens) are a potential reservoir for the Pasteurella multocida bacterium that causes avian cholera, serum samples and/or pharyngeal swabs were collected from > 3,400 adult geese breeding on Wrangel Island (Russia) and Banks Island (Canada) during 1993-1996. Pharyngeal swab sampling rarely (> 0.1%) detected birds that were exposed to P. multocida in these populations. Geese with serum antibody levels indicating recent infection with P. multocida were found at both breeding colonies. Prevalence of seropositive birds was 3.5% at Wrangel Island, an area that has no recorded history of avian cholera epizootics. Prevalence of seropositive birds was 2.8% at Banks Island in 1994, but increased to 8.2% during 1995 and 1996 when an estimated 40,000-60,000 snow geese were infected. Approximately 50% of the infected birds died during the epizootic and a portion of the surviving birds may have become carriers of the disease. This pattern of prevalence indicated that enzootic levels of infection with P. multocida occurred at both breeding colonies. When no avian cholera epizootics occurred (Wrangel Island, Banks Island in 1994), female snow geese (4.7%) had higher antibody prevalence than males (2.0%).     

Experimental Infection of a North American Raptor,American Kestrel (Falco sparverius), with Highly Pathogenic Avian Influenza Virus (H5N1)

Several species of wild raptors have been found in Eurasia infected with highly pathogenic avian influenza virus (HPAIV) subtype H5N1. Should HPAIV (H5N1) reach North America in migratory birds, species of raptors are at risk not only from environmental exposure, but also from consuming infected birds and carcasses. In this study we used American kestrels as a representative species of a North American raptor to examine the effects of HPAIV (H5N1) infection in terms of dose response, viral shedding, pathology, and survival. Our data showed that kestrels are highly susceptible to HPAIV (H5N1). All birds typically died or were euthanized due to severe neurologic disease within 4–5 days of inoculation and shed significant amounts of virus both orally and cloacally, regardless of dose administered. The most consistent microscopic lesions were necrosis in the brain and pancreas. This is the first experimental study of HPAIV infection in a North American raptor and highlights the potential risks to birds of prey if HPAIV (H5N1) is introduced into North America.     

Dynamics of West Nile Virus Persistence in House Sparrows (Passer domesticus)

West Nile Virus (WNV) is now endemic throughout North America, with annual recurrence dependent upon successful overwintering when cold temperatures drive mosquito vectors into inactivity and halt transmission. To investigate whether avian hosts may serve as an overwintering mechanism, groups of eight to ten House Sparrows were experimentally infected with a WN02 genotype of WNV and then held until necropsy at 3, 5, 7, 9, 12, 15, or 18 weeks post-infection (pi) when they were assessed for the presence of persistent infection. Blood was collected from all remaining birds every two weeks pi, and sera tested for WNV RNA and WNV neutralizing antibodies. West Nile virus RNA was present in the sera of some birds up to 7 weeks pi and all birds retained neutralizing antibodies throughout the experiment. The detection of persistently infected birds decreased with time, from 100% (n = 13) positive at 3 weeks post-infection (pi) to 12.5% (n = 8) at 18 weeks pi. Infectious virus was isolated from the spleens of birds necropsied at 3, 5, 7 and 12 weeks pi. The current study confirmed previous reports of infectious WNV persistence in avian hosts, and further characterized the temporal nature of these infections. Although these persistent infections supported the hypothesis that infected birds may serve as an overwintering mechanism, mosquito-infectious recrudescent viremias have yet to be demonstrated thereby providing proof of principle.     

Experimental infections of waterfowl with Sphaeridiotrema globulus (Digenea)

Sphaeridiotrema globulus in experimentally infected mute swans (Cygnus olor), mallard ducks (Anas platyrhynchos) and Canada geese (Branta canadensis) induced ulcerative hemorrhagic enteritis. Sites of infection include the jejunum and ileum. The digeneans ulcerated the intestine. The inflammatory response was primarily lymphocytic with some eosinophils. Severe hemorrhage from damaged submucosal capillaries provided a blood meal for the parasite and caused anemia in the host. Extra-medullary hematopoiesis occurred in the liver, and an erythroid hyperplasia occurred in the bone marrow of infected birds. Infected birds exhibited muscular weakness and died from shock associated with severe blood loss. Mallards and Canada geese were less susceptible to fatal infection than the mute swan as evidenced by survivors in the higher dose groups.     

Genetically different isolates of Trypanosoma cruzi elicit different infection dynamics in raccoons (Procyon lotor) and Virginia opossums (Didelphis virginiana)

Trypanosoma cruzi is a genetically and biologically diverse species. In the current study we determined T. cruzi infection dynamics in two common North American reservoirs, Virginia opossums (Didelphis virginiana) and raccoons (Procyon lotor). Based on previous molecular and culture data from naturally-exposed animals, we hypothesised that raccoons would have a longer patent period than opossums, and raccoons would be competent reservoirs for both genotypes T. cruzi I (TcI) and TcIIa, while opossums would only serve as hosts for TcI. Individuals (n = 2 or 3) of each species were inoculated with 1 × 10⁶ culture-derived T. cruzi trypomastigotes of TcIIa (North American (NA) – raccoon), TcI (NA – opossum), TcIIb (South American – human), or both TcI and TcIIa. Parasitemias in opossums gradually increased and declined rapidly, whereas parasitemias peaked sooner in raccoons and they maintained relatively high parasitemia for 5 weeks. Raccoons became infected with all three T. cruzi strains, while opossums only became infected with TcI and TcIIb. Although opossums were susceptible to TcIIb, infection dynamics were dramatically different compared with TcI. Opossums inoculated with TcIIb seroconverted, but parasitemia duration was short and only detectable by PCR. In addition, raccoons seroconverted sooner (3–7 days post inoculation) than opossums (10 days post inoculation). These data suggest that infection dynamics of various T. cruzi strains can differ considerably in different wildlife hosts.     

Vertebrate host specificity of two avian malaria parasites of the subgenus Novyella: Plasmodium nucleophilum and Plasmodium vaughani

The susceptibility of wild-caught European passeriform birds to naturally isolated malaria parasites, Plasmodium (Novyella) nucleophilum and Plasmodium (Novyella) vaughani, was studied by means of intramuscular subinoculation of infected citrated blood. Plasmodium nucleophilum of the great tit, Parus major, was transmitted to 3 great tits, but 3 blackcaps (Sylvia atricapilla) were not susceptible. Plasmodium vaughani of the robin, Erithacus rubecula, was transmitted to 1 robin and 1 blackcap, but 1 dunnock, Prunella modularis, was not susceptible. The prepatent period was between 8 and 10 days in all experimental infections. Maximum experimental parasitemia (3.4% of red cells) was detected in great tits infected with P. nucleophilum 23 days postexposure. A light (<0.01%) transient parasitemia of P. vaughani developed in the robin and blackcap. This study is in accord with former experimental observations on host specificity of P. nucleophilum and P. vaughani, which are characterized by a wide, but selective, range of avian hosts. Two new host-parasite associations were recorded.     

Eimeria acervulina infection elevates plasma and muscle 3-methylhistidine levels in chickens

To assess muscle breakdown during avian coccidiosis, the level of the nonmetabolizable amino acid 3-methylhistidine (3MH) was determined in muscle, plasma and excreta from chickens infected with Eimeria acervulina. The changes in 3MH levels during infection were assessed at 1-29 days postinoculation (DPI) in animals given 5 x 10(5) oocysts per bird. The effect of levels of parasitism were evaluated at 8 DPI in birds receiving 5 x 10(3), 5 x 10(4), 5 x 10(5) or 1 x 10(6) oocysts each. The 3MH levels of plasma, muscle, and excreta samples were determined by high-pressure liquid chromatography after derivatization with fluorescamine. Weight gains, breast muscle weight, eviscerated weight, plasma carotenoid levels, dry weight of muscle, and gross lesion scores were also determined. Infected birds had significantly elevated plasma and muscle 3MH at 4 and 8 DPI following a single dose of E. acervulina. The increase in 3MH levels had an inverse relationship with the time course of weight gain and plasma carotenoid levels. Plasma and muscle 3MH levels returned to control values by 15 DPI and remained unchanged from control values through the remainder of the experiment (29 DPI). Breast weight was decreased in infected birds, but the ratio of breast weight to eviscerated body weight was unchanged. Excretion of 3MH decreased relative to controls at 4 and 8 DPI and returned to control levels on 15 DPI. The plasma and muscle levels of 3MH were related to severity of infection; however, levels of excreted 3MH were not. The results suggested that muscle breakdown, as assessed by plasma and muscle levels of 3MH, increased during the acute stage of E. acervulina infection. The underlying causes for this muscle breakdown was unclear but could involve a physiological response to anorexia and decreased food intake during the acute phase of infection. Levels of excreted 3MH did not increase during infection and this may be the result of decreased excreta output during infection. Plasma and muscle levels of 3MH were correlated with severity of E. acervulina infections but may not be as sensitive an indicator of infection as plasma carotenoid levels or other physiological parameters.