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Eimeria is an intracellular obligate apicomplexan parasite that parasitizes the intestinal epithelial cells of livestock and poultry, exhibiting strong host and tissue tropism. Parasite-host interactions involve complex networks and vary as the parasites develop in the host. However, understanding the underlying mechanisms remains a challenge. Acknowledging the lack of studies on Eimeria invasion mechanism, we described the possible invasion process through comparative analysis with other apicomplexan parasites and explored the fact that parasite-host interactions serve as a prerequisite for successful recognition, penetration of the intestinal mechanical barrier, and completion of the invasion. Although it is recognized that microbiota can enhance the host immune capacity to resist Eimeria invasion, changes in the microenvironment can, in turn, contribute to Eimeria invasion and may be associated with reduced immune capacity. We also discuss the immune evasion strategies of Eimeria, emphasizing that the host employs sophisticated immune regulatory mechanisms to suppress immune evasion by parasites, thereby sustaining a balanced immune response. This review aims to deepen our understanding of Eimeria-host interactions, providing a theoretical basis for the study of the pathogenicity of Eimeria and the development of novel anticoccidial drugs., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Weng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Coccidiosis, an intestinal disease caused by Eimeria parasites, is responsible for major losses in the poultry industry by impacting chicken health. The gut microbiota is associated with health factors, such as nutrient exchange and immune system modulation, requiring understanding on the effects of Eimeria infection on the gut microbiota. This study aimed to determine the effects of Eimeria acervulina infection on the luminal and mucosal microbiota of the cecum (CeL and CeM) and ileum (IlL and IlM) at multiple time points (days 3, 5, 7, 10, and 14) post-infection. E. acervulina infection decreased evenness in CeL microbiota at day 10, increased richness in CeM microbiota at day 3 before decreasing richness at day 14, and decreased richness in IlL microbiota from day 3 to 10. CeL, CeM, and IlL microbiota differed between infected and control birds based on beta diversity at varying time points. Infection reduced relative abundance of bacterial taxa and some predicted metabolic pathways known for short-chain fatty acid production in CeL, CeM, and IlL microbiota, but further understanding of metabolic function is required. Despite E. acervulina primarily targeting the duodenum, our findings demonstrate the infection can impact bacterial diversity and abundance in the cecal and ileal microbiota., (© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

The purpose of this pilot study was to evaluate and determine the concentration of prostaglandin GF2α (PGF2α) and isoprostane 8-iso-PGF2α in plasma and intestine of specific pathogen-free (SPF) Leghorn chickens challenged with Eimeria maxima, with or without dietary supplementation of curcumin using solid-phase microextraction and ultra-performance liquid chromatography/tandem mass spectrometry. Eighty 1-day-old male SPF chickens were randomly allocated to one of four groups with four replicates (n = 5 chickens/replicate). Groups consisted of: (1) Control (no challenge), (2) Curcumin (no challenge), (3) Eimeria maxima (challenge), and (4) Eimeria maxima (challenge) + curcumin. At day 28 of age, all chickens in the challenge groups were orally gavaged with 40,000 sporulated E. maxima oocysts. No significant differences (P > 0.05) were observed in the groups regardless of the treatment or challenge with E. maxima. Enteric levels of both isoprostane 8-iso-PGF2α and PGF2α at 7 days and 9 days post-challenge were significantly increased (P < 0.01) compared to the non-challenge control chickens. Interestingly, the enteric levels of both isoprostane 8-iso-PGF2α and PGF2α at 7 days post-challenge were significantly reduced in chickens fed curcumin, compared to control chickens challenge with E. maxima. At 9 days post-challenge, only levels of isoprostane 8-iso-PGF2α in the enteric samples were significantly reduced in chickens challenged with E. maxima supplemented with curcumin, compared with E. maxima challenge chickens. No differences of isoprostane 8-iso-PGF2α or PGF2α were observed in plasma at both days of evaluation. Similarly, no significant differences were observed between the challenge control or chickens challenge with E. maxima and supplemented with curcumin at both times of evaluation. The results of this pilot study suggests that the antioxidant anti-inflammatory properties of curcumin reduced the oxidative damage and subsequent intestinal mucosal over-production of lipid oxidation products. Further studies to confirm and extend these results in broiler chickens are required.

Coccidiosis is one of the most prevalent diseases seen in the poultry industry leading to excessive economic losses. The aim of this study was to investigate the effect of butyric acid glycerol esters (BE) on the ileal and cecal microbiota in birds challenged with Eimeria maxima (EM). Ross 708 male broilers were fed a diet supplemented with 0 (control) or 0.25% BE from day 1. On day 21, half of the birds were infected with 10 3  EM oocysts. For determing microbiota, ileal and cecal contents and epithelial scrapings were collected at 7 and 10 D postinfection (PI). Alpha diversity of bacterial communities was mostly affected (P < 0.05) by time PI and EM infection. The richness of luminal bacterial populations in the ileum and ceca was affected (P < 0.05) by addition of BE and by time PI × EM × BE interaction, respectively. In the ileal and cecal luminal and mucosal bacterial communities, permutational multivariate analysis of variance (PERMANOVA, unweighted UniFrac) showed significant (P < 0.05) differences because of time PI and interaction between time PI, EM, and BE. Significant (P < 0.05) differences in taxonomic composition at the family level were observed in microbiota of luminal and mucosal populations of the ileum and ceca owing to time PI, EM, BE, and their interactions. The bacterial community present in the cecal lumen was characterized by the lowest number of differential bacteria, whereas the cecal mucosal community was characterized by the highest number of differentially abundant bacteria. In conclusion, our results show that EM infection and time PI has the biggest impact on microbial diversity in the chicken gut. The presence of BE in the diet had a limited effect on gut microbiota., (Copyright © 2020. Published by Elsevier Inc.)

Coccidiosis is caused by protozoa of the genus Eimeria. These are intracellular parasites of enterocytes that rupture the host cell, causing lesions in the intestinal mucosa. The lesions caused by Eimeria reduce nutrient absorption capacity, negatively affecting productive gains in broilers, and representing a gateway for other enteropathogens. The objective of this study was to analyze the correlation between lesions caused by Eimeria and the prevalence of coccidiosis and other alterations found in the gastrointestinal tracts of broilers produced in Brazil from 2017 to 2018. Intestinal health evaluations were performed in 32 integrations (farm) of broilers in Brazil, totaling 726 birds analyzed between the ages of 22 and 40 days. Necropsied chickens were collected at three different points, with at least three birds per shed. We analyzed the following changes in the gastrointestinal tract: presence of cellular desquamation, fluid and mucus excess, ingestion of bedding, small and large intestine lesion, food passage, altered tone, "Turkish towel" lesions, worm infection, enteritis and gizzard erosion. The definition of macroscopic lesion scores caused by Eimeria acervulina, Eimeria maxima, Eimeria tenella followed a specific methodology. Mucosal oocyst counts for E. maxima (E. maxima micro) was performed using an optical microscope with a magnification of 100×. We found that the species E. acervulina had the highest prevalence (5.5%). With respect to E. acervulina, a positive correlation was observed with cellular desquamation, bedding ingestion and passage of food. The second highest prevalence was E. maxima (average of 4%), showing positive correlations with cellular desquamation, fluid excess, bed ingestion, feed passage and E. acervulina. E. tenella represented the lowest prevalence (0.8%) among the species of Eimeria analyzed, showing a positive correlation with altered intestinal tone. On microscopic evaluation, E. maxima was present in 45% of mucosa scrapings, representing subclinical coccidiosis of 1125% (11.25-fold) greater than the rate of clinical coccidiosis. Regarding other alterations that were visualized in the gastrointestinal tract, we have recorded the incidence of altered intestinal tone (0.1%), worm infection (0.4%), small intestine (0.8%), enteritis (1%), duodenitis (1.5%), "Turkish towel" lesions (3.3%), excess fluid (4.5%), bed ingestion (6.9%), excess mucus (8.4%), food passage (10.3%), cellular desquamation (11%) and gizzard erosion (13.4%). We conclude that monitoring is of paramount importance to understand the intestinal health status of poultry lots. Microscopic E. maxima is present in 45%. We identified factors that correlate with reduction in intestinal health, impairing zoo-economic performance., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Up to now, four coccidian species have been identified in Rallidae (Aves: Gruiformes): Eimeria mongolica, E. alakuli, E. paludosa and E. porphyrulae. Here, we described an Eimeria species, E. paludosa, from a common gallinule (Gallinula galeata) in Mexico. Oocysts were ovoid and wall pitted single-layered. A prominent micropyle was present, the oocyst residuum absent and the polar granule was present. On histological examination of tissues, endogenous stages (meronts, microgametocytes and macrogametocytes) were seen in the epithelial cells of the small intestine (upper and lower intestine). In addition to a new locality, this is the first description of E. paludosa from G. galeata and is the third description of a coccidian infecting Rallidae in the Americas.

Three-week-old turkey poults were infected with pure lines of three species of Eimeria ( E. adenoeides , E. gallopavonis , and E. meleagrimitis ) recently isolated from commercial turkey farms. The lines had been propagated from a single oocyst and identified by species-specific PCR amplification of the mitochondrial cytochrome c oxidase subunit I (COI) gene. Five to six days after infection their intestines were removed and examined for the presence of intestinal lesions. A description and review of the pathology caused by these parasites is provided, and a scoring system developed by which the severity of the lesions can be evaluated. The system is similar to that described by Johnson, J. and Reid, W. M. [1970. Anticoccidial drugs: lesion scoring techniques in battery and floor-pen experiments with chickens. Experimental Parasitology , 28, 30-36] for chickens in which a score of zero to four is assigned to lesions of increasing severity. The intestinal lesions observed here, and their assigned scores, are supported by representative illustrations. It is hoped that they may prove a useful tool for evaluating the pathology caused by E. adenoeides , E. gallopavonis , and E. meleagrimitis in the turkey. RESEARCH HIGHLIGHTS A scoring system has been developed for intestinal lesions caused by three species of Eimeria that infect the turkey.The lesions attributable to these species are illustrated.

Eimeria species are intestinal protozoan parasites that cause lack of production, malabsorption and mortality in floor raised chickens. Administering an oral antibody to interleukin 10 (aIL-10) reduces the symptoms of coccidiosis in broilers, indicating interleukin 10 (IL-10) is key to Eimeria pathology. IL-10 is an anti-inflammatory cytokine and acts as a stand down signal to reduce inflammation and host pathology during disease. Related protozoan parasites exploit IL-10 to reduce pathogen-damaging host inflammatory responses. We hypothesize that IL-10 is increased during Eimeria infection through an unknown host-pathogen interaction, and by feeding aIL-10 to neutralize excess IL-10 the bird is allowed to mount an effective immune response to Eimeria. To determine the effects of aIL-10 during the intestinal immune response, intestinal pathology and the relationship between IL-10, interferon gamma (IFNγ) and Eimeria infection were evaluated in this study. In both experiments, broilers were administered either a 10x dose of Advent® Eimeria vaccine or saline. Duodenum, jejunum and cecum samples were collected, processed, stained and examined under a microscope. Evaluation of intestinal histomorphology during aIL-10 administration showed minimal differences in birds fed aIL-10 during infection compared to animals fed a control antibody during Eimeria infection. To further evaluate aIL-10's positive effect during infection, immunofluorescent histochemistry was performed on chicken intestines days 3-7 post Eimeria infection for IL-10 and IFNγ presence in intestinal mucosa in control and infected birds, in regions with and without visible Eimeria burden. IL-10 and IFNγ had significant changes between days 4.5-7 post-infection in birds fed aIL-10 compared to animals fed a control antibody. Overall we found that the duodenum had increased IL-10 presence and increased IFNγ presence, and the jejunum and cecum had decreased IL-10 presence and decreased IFNγ presence. These differences in spatial regulation of IL-10 and IFNγ may indicate Eimeria species induce slightly different cytokine responses., (Published by Elsevier B.V.)

Ovine Eimeria spp. infections cause increased mortality, reduced welfare and substantial economic losses, and anticocccidials are important for their control. Recent reports of anticoccidial resistance against ovine Eimeria spp. necessitate the development of in vitro methods for the detection of reduced anticoccidial efficacy, especially since the in vivo methods are both expensive, time consuming and requires the use of otherwise healthy animals. The aim of the present study was therefore to approach a preliminary standardization of in vitro assays for evaluation of the efficacy of the most commonly used anticoccidials in ruminants. For this purpose, apart from the evaluation of inhibition of oocyst sporulation, most effort was concentrated on assessment of the capacity of the different anticoccidials to inhibit both the invasion and further development (up to the first schizogony) of E. ninakohlyakimovae sporozoites in bovine colonic epithelial cells (BCEC). For this purpose, infected cultures were monitored 1, 8 and 15 days post infection to determine the infection rate, number of immature schizonts and number, size and appearance of mature schizonts, respectively. No clear inhibitory effect was found with any of the anticoccidial formulations tested, and we could not identify why there were no measurable effects from the different anticoccidials. Despite the lack of positive results, further investigations should be encouraged, as this could decrease the need for animal experiments and could be used in the initial assessment of anticoccidial efficacy of new drugs., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Differentiating the Eimeria species causing cecal coccidiosis in turkeys is challenging. To obtain benchmark biological data for Eimeria gallopavonis Hawkins 1952 and Eimeria meleagridis Tyzzer 1929 and to support the stability of the species concept for each, genetically typed, single oocyst-derived lines of E. gallopavonis Weybridge strain and E. meleagridis USAR97-01 were used to redescribe the biological, pathological, and morphological features of these parasites. Oocysts of E. meleagridis and E. gallopavonis overlap in dimensions, but oocysts of the former have a single polar granule compared with multiple in the latter. Mature first-generation meronts of E. gallopavonis were observed histologically as early as 48 h post-inoculation alongside the villi in jejunum (before and after Meckel's diverticulum), ileum, cecal neck and rectum, but not cecal pouches. Three asexual cycles were observed suggesting that early workers apparently overlooked one asexual cycle. Examination of endogenous development of a culture labeled "Eimeria adenoeides Weybridge strain" suggested that this strain (found in a number of publications as a large oocyst strain of "Eimeria adenoeides") matched the species description of E. gallopavonis and so has been renamed herein. Macroscopic lesions induced by E. gallopavonis consisted of caseous material distally from posterior of the yolk stalk through the remaining intestinal tract, excluding the cecal pouches. For E. meleagridis, only the first asexual generation was observed outside of the cecal pouches within the jejunum around the yolk stalk. Second- and 3rd-generation asexual stages developed almost exclusively in the cecal pouches (but not cecal necks). Macroscopic lesions described for E. meleagridis were similar to those of E. adenoeides. Marked corrugation of the cecal serosal surface was observed. Cecal pouches contained creamy colored, caseous material varying from loose material to granular. Distinguishing features of the Eimeria species infecting the lower part of the small intestine are summarized in the present study, and new type specimens were designated for E. gallopavonis and E. meleagridis to provide a stable reference for future work with these parasites.

The endogenous life cycle of Eimeria caliginosa was studied in experimentally infected dusky rice rats, Melanomys caliginosus. All endogenous stages were located in the epithelial cells of villi in the small intestine. Both Giemsa-stained mucosal scrapings and histological sections were studied for the diagnosis of all the life-cycle stages. Eimeria caliginosa has 3 generations of meronts (M) that differ by size, shape, and number of merozoites (m), which also differ in their size, shape, and location of their nuclei within the cytoplasm of the meronts. The 3 meront types, M 1 -M 3 , respectively, had 20-33 (m 1 ), 5-9 (m 2 ), and 13-16 (m 3 ) merozoites. Macrogametocytes and microgametocytes, as well as macrogametes and microgametes, completed the sexual cycle, which concludes with the formation of unsporulated oocysts. This parasite's endogenous development produced severe intestinal lesions in the experimentally infected dusky rice rats. In our ongoing work to understand the biodiversity present in plants and animals of the protected Reserva Biológica Alberto Manuel Brenes (ReBAMB) field station in Costa Rica, we now have discovered 3 new Eimeria species, and this is the second complete life cycle in which we document both the asexual and sexual stages.

Intracellular generation of nitric oxide (NO) and superoxide anion (SOA) can result in the formation of 3'-nitrotyrosine proteins (NTp). Nitrated proteins usually are associated with significant perturbation in protein function, apoptosis, autophagy, and cell death. We undertook the present study to establish the temporal dynamics of NTp generation in cytokeratin-18-positive epithelial cells (ETCs) of broiler chickens in response to infection with Eimeria acervulina. Duodenal tissue was harvested from noninfected (NOI) and infected (INF) broilers on days (d) 1, 3, 6, 7, and 10 postinfection (PI) and fixed, embedded, and sectioned for quantitative image analysis, immunohistochemistry with antibodies specific to NTp and the SOA-generating enzyme xanthine oxidase (XO). The pixel density characteristics for NTp and XO representative of ETCs demonstrated that NTp and XO increased in intestinal villi as early as d1 PI (P < 0.05 vs. NOI). Progressive increases in NTp were evident in ETCs through d6 PI. For XO, increases in cell content increased only through d3. On d6 and d7 PI, high levels of NTp were present in immune infiltrating cells (IIC) where no XO was detected. The increases in ETC NTp occurred in a defined pattern, significant by villus-to-crypt location for day of infection, initiating in the distal villus and progressing down into the crypts. Two NTp patterns were observed for ETCs: a high level associated with ETCs harboring parasites and a low-level increase in ETCs not containing Eimeria but in proximity to such. The data suggest that NTp and XO responses may mediate some of the processes through which ETCs respond to Eimeria to limit the extent of infection by this pathogen.

Rabbit coccidiosis is caused by infection with one or usually several Eimeria species, parasitizing in hepatobiliary ducts or intestinal epithelium of rabbits. To date, 11 species of rabbit coccidia have been well documented. Here we report a new species of Eimeria from rabbits. Sporulated oocysts were ellipsoidal to slightly ovoidal, 37.4 (32.6-41.2) μm in length, 23.5 (20.9-25.5) μm in width, with a shape index (length/width) 1.6 (1.43-1.91) and smooth, bilayered, homogeneously thick wall. The micropyle was obvious and with an inner diameter of 6.2 (5.0-7.5) μm. Both oocyst residuum and polar granule were absent. Sporocysts were ellipsoidal to elongate, 17.2 (13.2-20.0) μm long and 8.4 (7.5-9.1) μm wide, with a shape index (length/width) of 2.1 (1.74-2.21) and the presence of Stieda body and sporocyst residuum. The prepatent period was 132h. Phylogenetic analysis showed that 18S rDNA sequence of the new species clustered together with the 11 rabbit Eimeria species into a clade. However, ITS-1 sequence of the new species shared low similarities (27.1%-30%) with those of 11 rabbit Eimeria species. As the data above supported the erection of a new species, we named it as Eimeria kongi n. sp., in honor of Fanyao Kong, a Chinese parasitologist. The finding of the new species has important implications for the diagnosis and prevention of rabbit coccidiosis., (Copyright © 2017. Published by Elsevier B.V.)

This study used morphological techniques to describe and name four new species of coccidia from the brown kiwi (Apteryx mantelli). Four distinct eimerian oocyst species were recovered that we describe as new species. The largest of these, Eimeria paraurii n. sp. measured 32.2 × 19.8 μm and is morphologically similar to gametocytes previously described histologically in colorectal polyps (Morgan et al. in Parasitol Res 111(4):1689-1699, 2012). Eimeria apteryxii n. sp. measured 23.9 × 14.9 μm and is similar to renal oocysts described histologically in brown, rowi (A. rowii) and Haast tokoeka kiwi (A. australis "Haast") (Morgan et al. in Avian Pathol 42(2):137-146, 2013). Eimeria kiwii n. sp. measured 14.8 × 13.9 μm and resembled gametocytes described previously in kiwi intestinal epithelial cells in brown kiwi (Morgan et al. in Parasitol Res 111(4):1689-1699, 2012). Eimeria mantellii n. sp. measured 17.8 × 10.7 μm and did not appear similar to any coccidia previously described in histological studies in kiwi. These are the first species of Eimeria to be described and named from brown kiwi. Because the morphological descriptions in the present study were determined from a limited number of kiwi droppings from two geographical locations, it is likely that these represent only a portion of Eimeria species present in other populations of both brown kiwi and other Apteryx species from around New Zealand.

The genus Eimeria (Apicomplexa, Coccidia) provides a wide range of different species with different hosts to study common and variable features within the genus and its species. A common characteristic of all known Eimeria species is the oocyst, the infectious stage where its life cycle starts and ends. In our study, we utilized Eimeria nieschulzi as a model organism. This rat-specific parasite has complex oocyst morphology and can be transfected and even cultivated in vitro up to the oocyst stage. We wanted to elucidate how the known oocyst wall-forming proteins are preserved in this rodent Eimeria species compared to other Eimeria. In newly obtained genomics data, we were able to identify different gametocyte genes that are orthologous to already known gam genes involved in the oocyst wall formation of avian Eimeria species. These genes appeared putatively as single exon genes, but cDNA analysis showed alternative splicing events in the transcripts. The analysis of the translated sequence revealed different conserved motifs but also dissimilar regions in GAM proteins, as well as polymorphic regions. The occurrence of an underrepresented gam56 gene version suggests the existence of a second distinct E. nieschulzi genotype within the E. nieschulzi Landers isolate that we maintain., (© S. Wiedmer et al., published by EDP Sciences, 2017.)

Metabolic and morphometric alterations of the duodenal villi caused by parasitism of chickens by Eimeria maxima were evaluated, using 100 male Cobb birds, randomly distributed into two groups (control and infected). The infected group was inoculated with 0.5 ml of a solution containing 5 × 10³ sporulated oocysts of Eimeria maxima. Ten birds per sample were sacrificed on the 6th, 11th, 22nd and 41st days post-infection (dpi). In order to evaluate the alterations, samples of duodenum, jejunum and ileum fragments were collected after necropsy for histological analysis. Villus biometry was determined by means of a slide graduated in microns that was attached to a binocular microscope. To evaluate the biochemical data, 5 ml of blood were sampled from the birds before sacrifice. The statistical analyses were performed using the GraphPad 5 statistical software for Windows. Tukey's multiple comparison test (p <0.05) was performed for the different dpi's and the unpaired t test for the difference between the groups. Infection by E. maxima causes both qualitative and quantitative alterations to the structure of the intestinal villi, thereby interfering with the absorption of nutrients such as calcium, phosphorus, magnesium, protein and lipids, with consequent reductions in the birds' weights.

Innate immune reactions conducted by macrophages may affect the outcome of primary infections and are crucial for the transition to adaptive immune responses. In bovine coccidiosis little is known on early monocyte/macrophage-mediated responses. We therefore investigated in vivo, in vitro and ex vivo reactions of monocytes and macrophages against Eimeria bovis, one of the most pathogenic Eimeria species in cattle. Macrophages significantly infiltrate the gut mucosa of E. bovis-infected calves, particularly after challenge infection. Furthermore, peripheral monocytes of infected animals, as precursor cells of macrophages, exhibited enhanced ex vivo phagocytic and oxidative burst activities. Enhanced levels of both activities were found early after infection and towards the end of first merogony. In vitro exposure of macrophages to sporozoites led to phagocytosis of the pathogen, whilst monocytes failed to do so. Phagocytosis occurred independently of the viability of the sporozoites, indicating that active invasion by the parasites was negligible. Phagocytosis occurred in the absence of immune serum, but could clearly be enhanced by addition of immune serum, suggesting macrophage-derived antibody-dependent cytotoxicity. Furthermore, co-culture of macrophages with sporozoites and stimulation with merozoite I antigen induced distinct levels of cytokine and chemokine gene transcription. Thus, the transcription of genes encoding for IFN-gamma, IL-12, TNF-alpha, IL-6, CXCL1, CXCL8, CXCL10 and COX-2 was upregulated after sporozoite encounter. In contrast, soluble merozoite I antigen only induced the gene transcription of IL-6 and IL-12 and failed to upregulate IFN-gamma and TNF-alpha gene transcripts. In monocytes, IFN-gamma and CXCL10 were found upregulated, all other immunoregulatory molecules tested were not affected. In summary, our results strongly suggest that macrophage-mediated, innate immune reactions play an important role in the early immune response to E. bovis infections in calves.

Although chronic intestinal helminth infections may suppress allergen-induced airway pathology by inducing a combination of modified T-helper (Th) 2 and immunosuppressive cytokines, a similar capacity of natural acute intestinal infections has remained untested, despite their global prevalence. Here, we show that allergic airway phenotypes including eosinophilia, eotaxin mRNA, and Th2 cytokines are significantly suppressed in animals that were infected by and that have cleared the intestinal parasite Eimeria vermiformis. Unlike in helminth-infected animals, regulation requires temporal coincidence of infection with sensitization; depends on interferon-gamma; and is not associated with an enhanced antigen-specific immunoglobulin G1 response. Moreover, regulation was effective following allergen sensitization in different anatomical sites, and in young and adult mice. These data highlight a transient anatomical dissemination of "functional immunologic dominance" following infection of the gut mucosa. They strongly support the hypothesis that airway allergies are naturally suppressed by both acute and chronic mucosal pathogens, but by different mechanisms.

A case of coccidiosis in a young, red male squirrel (Sciurus vulgaris L.) has been described in this report. The squirrel was found dead and presented to the department of pathology for necropsy. A traumatic lesion was observed on the face that could have caused death. At necropsy the large and small intestines were swollen due to fluid and gas. During the examination of gut content numerous coccidia oocysts were observed. After sporulation, the oocysts were identified as those of Eimeria lancasterensis. In the histopathological examination numerous coccidia developmental stages were observed in the epithelium of small intestine. This is the first report of Eimeria lancasterensis identification in squirrels in Turkey.

To investigate the influence of genetic differences in the MHC on susceptibility to avian coccidiosis, M5.1 and M15.2 B-haplotype-disparate Fayoumi chickens were orally infected with live Eimeria maxima oocysts, and BW gain, fecal oocyst production, and expression of 14 immune-related genes were determined as parameters of protective immunity. Weight loss was reduced and fecal parasite numbers were lower in birds of the M5.1 line compared with M15.2 line birds. Intestinal intraepithelial lymphocytes from M5.1 chickens expressed greater levels of transcripts encoding interferon-gamma (IFN-gamma), interleukin-1beta (IL-1beta), IL-6, IL-8, IL-12, IL-15, IL-17A, inducible nitric oxide synthase, and lipopolysaccharide-induced tumor necrosis factor-alpha factor and lower levels of mRNA for IFN-alpha, IL-10, IL-17D, NK-lysin, and tumor necrosis factor superfamily 15 compared with the M15.2 line. In the spleen, E. maxima infection was associated with greater expression levels of IFN-gamma, IL-15, and IL-8 and lower levels of IL-6, IL-17D, and IL-12 in M5.1 vs. M15.2 birds. These results suggest that genetic determinants within the chicken MHC influence resistance to E. maxima infection by controlling the local and systemic expression of immune-related cytokine and chemokine genes.

The progression of coccidiosis provoked by Eimeria acervulina was followed in chicks fed on OTA-contaminated as well as on OTA-free diets. More heavy progress of duodenal coccidiosis, including mortality, occurred in OTA-treated chicks as can be seen from the higher value of lesion (3.50) and oocyst (31.65) indices. A stronger decrease of serum total protein was found in OTA-treated chicks (22.80 g/l) than in chicks infected with E. acervulina(24.20 g/l), but that decrease was strongest in chicks treated with OTA and simultaneously infected with E. acervulina (19.71 g/l). The serum concentration of uric acid was significantly increased in all chicks exposed to OTA, most notably in those additionally infected with E. acervulina (1020.6 (micro mol/L), whereas the serum enzyme activity of AST was increased only in chicks infected with E. acervulina and highest in those fed OTA contaminated diet (122.2 U/L). OTA induced degenerative changes in kidneys, liver and heart as well as a depletion of lymphoid tissue in the lymphoid organs and a decrease of body weight. Coccidiosis induced only a slight growth depression and duodenal hemorrhages in addition to characteristic duodenal damages. The impairment of kidney function, histopathological changes and general growth depression were stronger when chicks infected with E. acervulina were also given OTA.

Coccidiosis, a major intestinal parasitic disease of poultry, induces a cell-mediated immune response against the etiologic agent of the disease, Eimeria. In the current study, the expression levels of gene transcripts encoding pro-inflammatory, Th1, and Th2 cytokines, as well as chemokines were measured in intestinal intraepithelial lymphocytes (IELs) after Eimeria maxima infection. In addition, changes in IEL numbers were quantified following E. maxima infection. Transcripts of the pro-inflammatory and Th1 cytokines IFN-gamma, IL-1beta, IL-6, IL-12, IL-15, IL-17, and IL-18 were increased 66- to 8 x 10(7)-fold following primary parasite infection. Similarly, mRNA levels of the Th2 cytokines IL-3, IL-10, IL-13, and GM-CSF were up-regulated 34- to 8800-fold, and the chemokines IL-8, lymphotactin, MIF, and K203 were increased 42- to 1756-fold. In contrast, IFN-alpha, TGF-beta4, and K60 transcripts showed no increased expression, and only the level of the Th2 cytokine IL-13 was increased following secondary E. maxima infection. Increases in intestinal T cell subpopulations following E. maxima infection also were detected. CD3(+), CD4(+), and CD8(+) cells were significantly increased at days 8, 6, and 7 post-primary infection, respectively, but only CD4(+) cells remained elevated following secondary infection. TCR1(+) cells exhibited a biphasic pattern following primary infection, whereas TCR2(+) cells displayed a single peak in levels. Taken together, these data indicate a global chicken intestinal immune response is produced following experimental Eimeria infection involving multiple cytokines, chemokines, and T cell subsets.

Specific pathogen-free (SPF) rabbits were inoculated with oocysts of an original strain (OS) of Eimeria piriformis and the first newly developed oocysts recovered from the intestine were used for infection of other rabbits. The prepatent period (PP) was shortened after 12 passages from 194 to 170 hours and remained stable after 5 passages without any selection pressure. Oocysts of the precocious line (PL) exhibited peculiar morphology. Besides refractile bodies (RB) within sporozoites, one huge RB joined with a residual body was present inside each sporocyst. The parasite developed in the proximal colon and, to a lesser extent, in other parts of the large intestine. All stages were seen in the epithelium of crypts. In OS, four asexual generations preceded gamogony and, like in other rabbit coccidia, two types of meronts were observed: meronts of type A that develop into polynucleate merozoite, in which endomerogony takes place, and meronts of the type B that form uninucleate merozoites. The endogenous development of PL was identical with that of OS except for the last merogony which was absent. This resulted in earlier appearance of gamogony and shortening of PP. These observations of the life cycle of E. piriformis substantially improve on its description made 50-60 years ago.

The SPF rabbits were inoculated with oocysts of Eimeria flavescens and the first newly developed oocysts were recovered. They were used for inoculation of other rabbits which consequently excreted oocysts sooner than in the previous passage. By repeated use of this method, the prepatent period was shortened after 18 passages by more than 60 h. The endogenous development of this precocious line (PL) differed from that of the original strain (OS). Compared to OS, two asexual generations, second (or third) and fourth, were absent in PL. The first merogony took place in the jejunum and ileum in OS and, in contrast, in the large intestine in PL. Like in other rabbit coccidia, two types of meronts (A and B) were seen in each generation. However, the ratio of B: A meronts in the last (fifth) asexual generation as well as ratio of microgamonts:macrogamonts differs in OS and PL.

Intraepithelial lymphocytes (IELs) play a critical role in protective immune response to intestinal pathogens such as Eimeria, the etiologic agent of avian coccidiosis. A list of genes expressed by intestinal IELs of Eimeria-infected chickens was compiled using the expressed sequence tag (EST) strategy. The 14,409 ESTs consisted of 1851 clusters and 7595 singletons, which revealed 9446 unique genes in the data set. Comparison of the sequence data with chicken DNA sequences in GenBank identified 125 novel clones. This EST library will provide a valuable resource for profiling global gene expression in normal and pathogen-infected chickens and identifying additional unique immune-related genes.

The initial phases of invasion of mammalian coccidia of the genus Eimeria into host tissue are still poorly known. This process, including the passage of oocysts through the intestinal lumen, excystation of sporozoites, their penetration into epithelial cells and migration to the target site was studied in both naive and immune mice infected with Eimeria falciformis. After oral infection, the intact oocysts were transported with enteral contents to the large intestine, where the excystation of sporozoites and their penetration into superficial epithelium took place. The sporozoites subsequently migrated into the epithelium of crypts, which is the specific site of asexual multiplication. The immune status of the hosts did not affect the passage of oocysts, excystation and penetration of sporozoites. However, the migration of sporozoites towards their target site (crypts) was impeded in immune mice and sporozoites tended to remain in superficial mucosa rather than migrate to the crypts.

To study the pathophysiology of diarrhoea in coccidial infections, Na+ and Cl- fluxes (J(Na), J(Cl)), short circuit current (I(sc)) and tissue conductance (g(t)) were determined in stripped gut epithelia of Eimeria separata infected rats employing the Ussing chamber technique. E. separata invades enterocytes of the caecum and proximal colon. Na+ absorption was generally reduced in infected tissues, Cl- absorption only in the caecum. I(sc) values were increased in the caecum and reduced in the proximal colon. Tissue conductance was not affected. Values tended to normal with time after infection. Theophylline caused markedly increased I(sc) and g(t) values in the caecum epithelia of infected rats. In the epithelia of the distal colon, i.e. the non-infested part of the large intestine, g(t) values remained unaffected but I(sc) was fourfold increased. This I(sc) increase was strongly sensitive to amiloride, suggesting a compensatory activation of Na+ channels in the distal colon of infected rats. Accordingly, serum levels of aldosterone, which activates Na+ channels in the distal colon, were increased to eightfold levels in infected animals. Thus compensatory Na+ absorption was under endocrine control.

The endogenous cycle of Eimeria flavescens was studied in specific pathogen-free rabbits by means of histology and transmission electron microscopy. In total, five asexual generations were observed and two types of meronts and merozoites were found in each generation. Type A gave rise to a smaller number of thick polynucleate merozoites in which daughter merozoites were formed by endomerogony, while in the type B meronts slender uninucleate merozoites arose from ectomerogony. The first generation meronts were found in the crypts and proximal part of the villi of the duodenum and jejunum, whereas the three following generations developed in the superficial epithelium of the large intestine (cecum, vermiform appendix and colon). The last merogony as well as gamogony took place in crypts of the large intestine.

Coccidia of the genus Eimeria are present in most pigs raised on dirt in the United States. They are generally considered nonpathogenic in weaned pigs. Oocysts of Eimeria spinosa Henry, 1931 were observed in tissue sections and intestinal contents of a weaned male pig that died suddenly on a farm in Iowa. Microscopically, necrotizing enteritis associated with many thick-walled coccidial oocysts was present in intestinal sections. Examination of intestinal contents demonstrated oocysts that were thick-walled and had small projections on the surface of the oocyst wall, characteristic of E. spinasa Henry, 1931 of swine. Twenty-live oocysts in intestinal contents measured 20.4 by 14.2 microm. No pathogenic bacteria were detected in the pig by culture methods, but lesions suggestive of salmonellosis were observed in some tissues. The specific cause of death was not determined; however, E. spinosa infection was considered to have contributed to the death of this pig. The results suggest that E. spinosa may be pathogenic for pigs.

An electron microscopic study of the endogenous development of Eimeria mulardi Chauve, Reynaud and Gounel, 1994 was carried out in mule ducks which are hybrids of the domestic duck (Anas platyrhynchos) and the muscovy duck (Cairina moschata). All of the endogenous stages were seen within the nucleus of the host cell. Merozoites arose from ectomerogony and three mutually similar merogonies were noted. The asexual stages were found in leukocyte-like cells in the lamina propria of the jejunum, ileum and caecum, while the gamonts developed in glandular epithelial cells in the same part of the intestine.

The phenotype of cells transporting sporozoites of Eimeria necatrix during a primary infection was determined using a panel of six monoclonal antibodies to various chicken lymphocyte surface markers. Sporozoites and cells harboring them were examined at 8, 12 and 18 h postinfection using two-color immunoflorescence and confocal microscopy. The majority of parasites observed within lymphocytes were found in CD 8 + (15%) or CD 3+ (13-22%) cells at all time periods examined. Smaller numbers were found within deltagamma TCR+ (5%) and alphabeta TCR+ (5%) lymphocytes. No sporozoites were found within CD 4+ or IgM+ lymphocytes at any of the time periods.

This study aimed to characterise the local (intestinal) immune response of rats after primary and challenge infections with Eimeria separata. Naive rats and rats which had been immunised by two moderate infections were exposed to a heavy infection with 100000 oocysts per animal. Necropsies were performed 0, 24 and 48 h after infection and lymphocyte subpopulations were microscopically quantified in the caecum mucosa after marking by immunohistological techniques. There was no difference between naive and immune rats concerning the number of CD45R(+) (B) cells, whereas significantly more CD3(+) (T) cells were found in the caecum wall of the immune rats. CD4(+) T cells predominated in animals after primary infection, whereas CD8(+) T cells represented the major T-cell subset in challenged rats. The proportion of TCRgammadelta(+) T cells did not differ in the mucosa between the groups examined, whereas challenged rats showed significantly increased numbers of TCRalphabeta(+) T cells in the caecum wall when compared with animals after a primary infection. Thus, CD4(+) T cells may be particularly involved in the immune response to a primary infection of rats with E. separata whereas immunity to a challenge infection seems to be mediated predominantly by CD8(+) and TCRalphabeta(+) T cells.

1. Coccidiosis, caused by different Eimeria species, is believed to be a more prominent problem in loose-housed layers kept on litter than in battery cages. In this study, the impact and development of Eimeria infections were investigated in layers kept in litter-based, high stocking density systems for loose-housed hens. 2. Layers from 57 flocks on 26 farms were followed by necropsy of a representative sample of birds that died or had to be culled. Coccidiosis was diagnosed in 11 flocks (19.3%) from 9 (31%) of the farms. The outbreaks occurred when the birds were 19 to 32 weeks old. E. maxima was identified in 6 and E. tenella in 3 of the outbreaks. 3. Sixteen of the flocks were also monitored with faecal and litter samples collected at regular intervals. Oocysts were detected in samples from all these flocks. The pattern of oocyst excretion was similar in most of the flocks, with maximum counts at 4 to 8 weeks after introduction to the laying house. There was no significant correlation between the levels of oocysts in faeces and clinical coccidiosis. 4. Raising pullets without any coccidiostat, to increase their chance to develop immunity against coccidia, was not found to decrease the risk of coccidiosis during the production period when compared to the practice of giving amprolium and ethopabate during the rearing period.

We examined exogenous and endogenous development of Eimeria procera in experimentally infected grey partridges (Perdix perdix). Our examination included data on morphology, localization, duration of schizogony and gametogony and morphology of sporulated oocysts. The endogenous stages of E. procera developed in large numbers within the epithelial cells of caecal crypts. The asexual development comprised three generations of schizonts. The first fully developed macrogametes and microgamonts were observed on Day 5 post-infection (p.i.) in histologic section. The patent period began on Day 6 p.i. and ended on Day 11 p.i. with peak production of oocysts on Days 7 and 8. Long oval oocysts of E. procera measured 25.78-28.13 microm in length and 14.06-15.24 microm in width, sporulation time ranged from 18 to 24h at 25 degrees C and from 36 to 48h at 20 degrees C.

Ten poultry farms (broiler breeder pullets, layer pullets, and broilers) in the provinces of Entre Rios and Buenos Aires in Argentina were examined for presence of Eimeria spp. Litter samples obtained from flocks 7-11 wk old were taken to the laboratory for oocyst counting and sporulation, then concentrated for inoculation into coccidia-free chickens. Species were identified by prepatent period, oocyst size, location and appearance of lesions in the intestine, microscopic examination of mucosal smears, and histology (to confirm Eimeria brunetti). On this basis, Eimeria praecox was found in two samples, Eimeria mitis in two, Eimeria acervulina in nine, Eimeria maxima in seven, Eimeria necatrix in three, Eimeria tenella in seven, and E. brunetti in four. These results confirm the presence of all seven recognized species of Eimeria in chickens in the Republic of Argentina.

Intestinal parasitism is a major stress factor leading to malnutrition and lowered performance and production efficiency of livestock and poultry. Coccidiosis is an intestinal infection caused by intracellular protozoan parasites belonging to several different species of Eimeria. Infection with coccidia parasites seriously impairs the growth and feed utilization of chickens and costs the US poultry industry more than $1.5 billion in annual losses. Although acquired immunity to Eimeria develops following natural infection, due to the complex life cycle and intricate host immune response to Eimeria, vaccine development has been difficult and a better understanding of the basic immunobiology of pertinent host-parasite interactions is necessary for developing effective immunological control strategies against coccidiosis. Chickens infected with Eimeria produce parasite specific antibodies in both the circulation and mucosal secretions but humoral immunity plays only a minor role in protection against this disease. Rather, recent evidence implicates cell-mediated immunity as the major factor conferring resistance to coccidiosis. This review will summarize current understanding of the avian intestinal immune system and its response to Eimeria as well as provide a conceptual overview of the complex molecular and cellular events involved in intestinal immunity to coccidiosis. It is anticipated that increased knowledge of the interaction between parasites and host immunity will stimulate the birth of novel immunological and molecular biological concepts in the control of intestinal parasitism.

The endogenous development of the rabbit coccidium Eimeria vejdovskyi was studied in SPF rabbits using light and electron microscopy. All endogenous stages were seen in the ileal epithelium. There were two types of meronts in each of five asexual generations. Type A produced fat, polynucleate merozoites while type B meronts had slender uninucleate merozoites. First- second- and third-generation meronts were in the crypts. The first meronts were at the bottom of the crypts, very often in the Paneth cells. The meronts of the fourth generation were in the middle of the villi; the fifth-generation meronts were recorded in the middle and at the top of the villi. The prepatent period was 10 days.

The ultrastructure of intracytoplasmic meronts and macrogamonts of Eimeria s.l. boveroi in the small intestine of the gekkonid lizard Hemidactylus mabouia from Belem, Para north Brazil is described. Young meronts, and some of the fully grown macrogamonts, are coated with a glycocalyx which, in cross-section, has the appearance of a series of fine tubules. The wall of the parasitophorous vacuole (PV) is a single membrane, lined on the host-cytoplasm side with an endoplasmic reticulum (ER) which sometimes expands into large cisternae filled with electron-lucent, globular material. The membranal edges of the ER, canaliculi and cisternae have regularly spaced indentations filled with an electron-dense substance. Vesicular mitochondria are present in addition to those of the conventional type. Macrogamonts develop the characteristic type 1 and type 2 wall-forming bodies, and in some zygotes the cisternae containing the latter are grossly expanded. Both types of wall-forming bodies persist in young oocysts that have a distinct oocyst wall.

The effect of betaine and salinomycin on absorption of methionine and glucose in tissue from the duodenal loops of Eimeria acervulina-infected chicks was determined. Differences in the ultrastructure of the intestinal cells and parasite developmental stages were also examined. With a drug-resistant isolate of E. acervulina, methionine absorption was significantly higher in chicks fed a basal diet supplemented with 0.15% betaine as compared with absorption in chicks fed the unsupplemented basal diet. Addition of 66 ppm salinomycin to the diet containing betaine did not further enhance absorption. Conversely, with a drug-sensitive isolate, methionine absorption was significantly higher in chicks fed a diet supplemented with both betaine and salinomycin than in chicks fed the unsupplemented basal diet. Tissue from chicks fed any of the supplemented diets was usually significantly heavier than that from chicks fed the unsupplemented diet, even when weight gains of the birds were similar. Glucose absorption was similar in all diet groups. Epithelial cells in coccidia-infected and uninfected chicks fed diets supplemented with betaine or betaine plus salinomycin were less electron dense than cells from chicks fed diets that were not supplemented with betaine. Merozoites of E. acervulina in chicks fed diets supplemented with salinomycin had extensive membrane disruption and vacuolization, but the damage was prevented when betaine was added to the diet. Numerous merozoites and intact schizonts were seen in the intestinal lumen of chicks fed the diet containing betaine plus salinomycin.

In the chronically inflamed ileum, unique mechanisms of alteration of transport processes suggest regulation by different immune-inflammatory mediator pathways. We previously demonstrated that Na+-glucose cotransport in the chronically inflamed ileum was inhibited by a decrease in cotransporter number without a change in glucose affinity. The aim of this study was to determine the alterations in Na+-amino acid cotransport in chronically inflamed ileum produced by coccidial infection in rabbits. [3H]alanine uptake was performed in cells and vesicles by rapid filtration. In villus cells from chronically inflamed ileum, Na+-K+-ATPase was reduced 50% and Na+-alanine cotransport was also reduced (5.8 +/- 1.2 in normal and 1.4 +/- 0.5 nmol/mg protein in inflamed; n = 6, P < 0.05). [3H]alanine uptake in brush-border membrane vesicles was reduced in chronically inflamed ileum (73.2 +/- 1.2 in normal and 21.5 +/- 3.2 pmol/mg protein in inflamed; n = 3, P < 0.05), suggesting a direct effect on the cotransporter itself. Na+-amino acid cotransport in chronically inflamed ileum was inhibited by a decrease in affinity without a change in the maximal rate of uptake, and unaltered steady-state mRNA levels also suggested that the number of cotransporters was unchanged. Thus the mechanisms of inhibition of Na+-amino acid cotransport and Na+-glucose cotransport in chronically inflamed ileum are different. These observations suggest that different immune-inflammatory mediators may regulate different transport pathways during chronic ileitis.

The effects of experimental infections with Eimeria tenella (Experiment 1, n = 144) or E. maxima (Experiment 2, n = 216) in broiler chickens fed whole wheat, with or without access to grit, as compared to a standard pelleted feed were studied. Inclusion of whole wheat was gradually increased up to 30% at 3 weeks of age. Grit was given separately. The chickens were kept on litter in a parasite-free environment with free access to water and feed. At 3 weeks of age half the number of chickens were individually inoculated with 500 sporulated oocysts of E. tenella (Experiment 1) or 3,000 sporulated oocysts of Eimeria maxima (Experiment 2), and the remaining birds were kept separate as uninfected controls. Neither coccidiostats nor growth enhancers were used. Oocyst concentration was determined from each group separately. Intestinal lesions were scored on 6 birds per feed regime 7 d postinoculation, and on the remaining birds at slaughter. Diet had no significant effect or bird performance during infection. However, there was an indication that the E. maxima infection had more negative effect on weight gain in birds given standard feed than in those given whole wheat supplement, but the difference was not significant (p < 0.09). The number of oocysts shed or mean intestinal lesion scores did not differ between diets in either experiment. In both experiments, the number of Clostridium perfringens was higher in the caeca of inoculated birds, but there were no differences between diets.

The endogenous development and prepatent and patent periods of Eimeria ninakohlyakimovae were studied in 43 1-3-wk-old coccidia-free kids inoculated with 5.0 x 10(4), 1.5 x 10(5), 2.0 x 10(5), or 9.0 x 10(5) sporulated oocysts/kg. Twenty-five kids were killed at 24- or 48-hr intervals, 2-18 days after inoculation (DAI). Two generations of meronts, gamonts, gametes, and oocysts were found in sections stained with hematoxylin and eosin and examined using under light microscopy. The first generation of meronts developed in the endothelium of the lacteals, in the lamina propria, and in the lymphatic vessels of the ileum submucosa. Mature, first-generation meronts, 165.5 x 123.6 microm, were first found 10 DAI. Second-generation merogony developed in the crypt epithelial cells of the cecum and colon; mature meronts, 16.8 x 11.6 microm, were first seen 12 DAI. Gametogenesis occurred in the cecum and colon epithelium; mature microgamonts (16.1 x 13.0 microm), microgametes, macrogametes (14.7 x 12.5 microm), and oocysts (18.3 x 13.3 microm) were seen at 13 DAI. The course of the infection was followed in 18 kids examined every day until 24 DAI. The prepatent period was 14.7 (13-17) days and the patent period 6.8 (4-10) days. The sporulation time at 30 C, with constant aeration, was 2-3 days.

Five experiments were conducted to investigate the production of nitric oxide (NO) and superoxide anion (O2-) during infections of chickens with the coccidial parasite, Eimeria maxima, in order to assess the importance of these free radical species in the pathogenesis of the infections. Nitric oxide production was estimated by analyzing NO2(-)+NO3-, stable metabolites of NO, in the plasma and intestinal mucosa. The potential for O2- production was estimated from activities of beta-nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in mucosal homogenates. Levels of NO2(-)+NO3- reached maximum values at about 6 d postinoculation, a time when mucosal damage was high and oocysts were being shed. The activity of NADPH oxidase in infected mucosa was also increased. Thus, at that time, there was a potential for oxidative destruction of mucosal tissue from these free radicals and their reaction products. Levels of NO2(-)+NO3- did not increase in a stepwise manner with increasing infective dose, suggesting that production of NO may be regulated post-transcriptionally by other factors elaborated by the immune response to infection, or may be controlled by substrate limitations. A comparison of two E. maxima strains indicated that the virulence of a strain was not directly related to NO production. Increased production of O2- due to increased NADPH oxidase activity during infection may cause a reduction in levels of carotenoid pigments that is unrelated to malabsorption.

Comparisons were made between microscopic lesion scores (MLSs) and gross lesion scores (GLSs) in sections from small intestine of broilers during three routine coccidiosis screenings. The duodenal and jejunal GLS were determined and recorded by different evaluators. During each screening, 2-cm sections of duodenum and jejunum were collected, and sections of intestine were then scored using a microscopic lesion scoring system. No correlation between MLS and GLS was observed in duodenum in two out of three coccidiosis screenings, and no correlation was observed between MLS and GLS in jejunum in three out of three screenings. Our findings demonstrate that, if used alone in coccidiosis screening, GLSs can underestimate infections and may not provide a true representation of the magnitude of Eimeria maxima infection within broiler flocks.

Vertebrate immune systems contain T cells bearing either alpha beta or gamma delta T-cell antigen receptors (TCRs). alpha beta T cells perform all well-characterized T-cell effector functions, while the biological functions of gamma delta + cells remain unclear. Of particular interest is the role of gamma delta + cells during epithelial infections, since gamma delta + cells are commonly abundant within epithelia. Eimeria spp. are intracellular protozoa that infect epithelia of most vertebrates, causing coccidiosis. This study shows that in response to Eimeria vermiformis, mice lacking alpha beta T cells display defects in protective immunity, while mice lacking gamma delta + cells display exaggerated intestinal damage, apparently due to a failure to regulate the consequences of the alpha beta T cell response. An immuno-downregulatory role during infection, and during autoimmune disease, may be a general one for gamma delta + cells.

Coccidia-free rabbits were inoculated with different doses of a pure strain of Eimeria coecicola and samples of gut were taken at 80, 96, 112, 128, 144, and 160 h postinoculation. The use of a very low infective dose (2-20 oocysts) was sufficient to study the last merogony. The number of merozoites in meronts increased when the infective dose decreased. Only the first merogony of this coccidium in lymphocytes or M-cells of gut-associated lymphoid tissue (GALT) has previously been described. Three other generations of meronts are described herein. All these endogenous stages were observed in the epithelium of the vermiform appendix, sacculus rotundus, and Peyer's patches, especially at the bases of the domes. However, in heavily infected tissues the gamonts were seen throughout the epithelium of the GALT. The third- and fourth-generation meronts were of two types. As in other eimerian species of the rabbit, type A meronts produced thick polynucleated merozoites, whereas type B meronts gave rise to large numbers of thin merozoites with one nucleus. Microgamonts were polynucleated and less numerous than macrogamonts. Type A meronts were also polynucleated and less numerous at the end of the merogony. Therefore, types A and B could correspond to a sexual phenotype differentiation occuring during the two asexual phases of multiplication.

Coccidian infection in Rana ridibunda and R. esculenta tadpoles was recorded in Hungarian fish farms. Oocysts enclosed in yellow bodies were found in the faeces and in the intestinal epithelium. Developmental stages also had intraepithelial sites. The species was identified with Eimeria neglecta Nöller, 1920; however, on the basis of its oocyst morphology it was transferred to the genus Goussia. Besides stages of Goussia neglecta n. comb., intranuclear trophozoites of another coccidian species were also recorded.

A new species of coccidium. Eimeria mulardi n. sp., has been described from the mule duck. The endogenous cycle is studied in experimentally infected ducks. A least two generations of meronts were observed, mainly in the lamina propria of jejunum and ileum and the gametogony occurred principally in glandular cells of the intestinal tract, except in duodenum. All the endogenous stages were localized in the nucleus of the cell.

When sporozoites of Eimeria tenella were inoculated into an isolated horn of the bicornuate caecum of the domestic fowl, replicating infections, culminating in the production of oocysts, were found, almost exclusively, in the inoculated horn. In contrast, sporozoites of E. tenella introduced into the bloodstream via a superficial vein induced infections of equivalent intensity in both horns of the caecum. These findings are discussed with reference to (1) the detection (by tissue transfer) of infective sporozoites in samples of cardiac blood and vascular tissues taken within 3 to 18 h of the oral inoculation of oocysts, and (2) the (previously published) observation that the sporozoites of E. tenella are transported from the superficial epithelium of the caecum (site of invasion) to the crypts (site of initial development) within host intra-epithelial lymphocytes. We suggest that a local inflammatory response to the invasion of sporozoites may be responsible for their re-location in proximity to the site of entry. This could act by directing the homing (or retention) of the parasite-bearing lymphocytes, and/or by providing a stimulus for the sporozoite to leave its transporting cell.