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The Clostridium-related poultry disease, necrotic enteritis (NE), causes substantial economic losses on a global scale. In the present study, a mixture of two plant-derived phytonutrients, Capsicum oleoresin and turmeric oleoresin (XT), was evaluated for its effects on local and systemic immune responses using a co-infection model of experimental NE in commercial broilers. Chickens were fed from hatch with a diet supplemented with XT, or with a non-supplemented control diet, and either uninfected or orally challenged with virulent Eimeria maxima oocysts at 14 d and Clostridium perfringens at 18 d of age. Parameters of protective immunity were as follows: (1) body weight; (2) gut lesions; (3) serum levels of C. perfringens α-toxin and NE B-like (NetB) toxin; (4) serum levels of antibodies to α-toxin and NetB toxin; (5) levels of gene transcripts encoding pro-inflammatory cytokines and chemokines in the intestine and spleen. Infected chickens fed the XT-supplemented diet had increased body weight and reduced gut lesion scores compared with infected birds given the non-supplemented diet. The XT-fed group also displayed decreased serum α-toxin levels and reduced intestinal IL-8, lipopolysaccharide-induced TNF-α factor (LITAF), IL-17A and IL-17F mRNA levels, while cytokine/chemokine levels in splenocytes increased in the XT-fed group, compared with the animals fed the control diet. In conclusion, the present study documents the molecular and cellular immune changes following dietary supplementation with extracts of Capsicum and turmeric that may be relevant to protective immunity against avian NE.

Background Species of the genus Eimeria cause coccidiosis in chickens, resulting in a huge burden to the poultry industry worldwide. Eimeria tenella is one of the most prevalent chicken coccidia in China, and E. tenella infection causes hemorrhagic cecitis. Methods Using an established model of coccidiosis in chickens combined with necropsy, imaging of pathological tissue sections, and other techniques, we evaluated the gross and microscopic lesions of cecal tissue within 15 days after inoculation with sporulated oocysts and described the endogenetic developmental process and relationship between E. tenella infection and enteritis development in chickens. Results We observed three generations of merogony and gamogony in E. tenella. We observed gross lesions in the cecum from 84 hpi (hours post inoculation) and microscopic lesions from 60 hpi. The lesions in the cecum mainly exhibited hemorrhagic enteritis. Their severity increased with the onset of the second generation of merogony. The lesions began to alleviate by the end of the endogenous stages of E. tenella. Conclusion We show, for the first time, the complete observation of a series of changes in enteritis caused by 5 × 103 E. tenella oocysts. This study provides reference materials for E. tenella research and pathological diagnosis. This study used necropsy, pathological tissue sections, and other techniques to evaluate the gross and microscopic lesions of cecal tissue in multiple periods within 15 days after incubation of sporulated oocysts. A model of necrotizing enteritis in chicken was developed by sporulated Eimeria tenella oocyst (5 × 103) infection. We observed in detail the process of merogony and sexual development in three generations of E. tenella, as well as the macroscopic lesions and histopathologic changes in the cecum that corresponded to their appearance.

Background In the animal production sector, enteritis is responsible for serious economic losses, and intestinal parasitism is a major stress factor leading to malnutrition and lowered performance and animal production efficiency. The effect of enteric parasites on the gut function of teleost fish, which represent the most ancient bony vertebrates, is far from being understood. The intestinal myxozoan parasite Enteromyxum leei dwells between gut epithelial cells and causes severe enteritis in gilthead sea bream (Sparus aurata), anorexia, cachexia, growth impairment, reduced marketability and increased mortality. Methods This study aimed to outline the gut failure in this fish-parasite model using a multifaceted approach and to find and validate non-lethal serum markers of gut barrier dysfunction. Intestinal integrity was studied in parasitized and non-parasitized fish by immunohistochemistry with specific markers for cellular adhesion (E-cadherin) and tight junctions (Tjp1 and Cldn3) and by functional studies of permeability (oral administration of FITC-dextran) and electrophysiology (Ussing chambers). Serum samples from parasitized and non-parasitized fish were analyzed using non-targeted metabolomics and some significantly altered metabolites were selected to be validated using commercial kits. Results The immunodetection of Tjp1 and Cldn3 was significantly lower in the intestine of parasitized fish, while no strong differences were found in E-cadherin. Parasitized fish showed a significant increase in paracellular uptake measured by FITC-dextran detection in serum. Electrophysiology showed a decrease in transepithelial resistance in infected animals, which showed a diarrheic profile. Serum metabolomics revealed 3702 ions, from which the differential expression of 20 identified compounds significantly separated control from infected groups in multivariate analyses. Of these compounds, serum inosine (decreased) and creatine (increased) were identified as relevant and validated with commercial kits. Conclusions The results demonstrate the disruption of tight junctions and the loss of gut barrier function, a metabolomic profile of absorption dysfunction and anorexia, which further outline the pathophysiological effects of E. leei.

Necrotic enteritis (NE) is an important infectious disease in chickens. Predisposing factors play critical roles both in disease outbreaks in the field and in models for experimental induction of disease. Systematic manipulation and study of predisposing factors help to optimize methods for the experimental reproduction of disease. The nature of such factors may play a confounding role in challenge models and, therefore, warrant investigation to determine their importance in industry-relevant NE reproduction models. In the present study, we examined the roles of dietary fishmeal inclusion, Eimeria inoculation (E), and Clostridium perfringens challenge (C) on broiler growth performance and induction of NE infection. The results showed that E, preceding C, greatly increased the severity of NE induced in broiler chickens, but fishmeal addition played only a marginal role in the challenge model. Bird performance was significantly affected by all three factors during the 35-day experimental period. Fishmeal increased body weight, but statistically significant effects of fishmeal were not observed on feed conversion ratio (FCR) and feed intake. Both Eimeria and C. perfringens significantly reduced body weight gain and feed intake. E but not C led to significantly poorer FCR. These findings indicate that dietary fishmeal may be removed from the model to allow the performance results of challenged chicks to be equivalent to the performance of chicks in the field. In conclusion, the present study demonstrates that an NE challenge model without fishmeal is valid and removes bird performance bias in the model introduced by feeding high fishmeal diets, refining the model to facilitate the yield of more commercially relevant results. Análisis multifactorial de la medida en que Eimeria y la harina de pescado predisponen a la enteritis necrótica en pollos de engorde. La enteritis necrótica (NE) es una enfermedad infecciosa importante en pollos. Los factores predisponentes juegan un papel crítico tanto en los brotes de enfermedades en el campo y en los modelos para la inducción experimental de la enfermedad. La manipulación sistemática y el estudio de los factores predisponentes ayudan a optimizar los métodos para la reproducción experimental de la enfermedad. La naturaleza de tales factores puede jugar un papel de confusión en modelos de desafío y por lo tanto, justifican una investigación para determinar su importancia en los modelos de reproducción de la enteritis necrótica que son relevantes para la industria. En el presente estudio se analizaron los efectos de la inclusión de harina de pescado en la dieta, la inoculación de Eimeria (E) y el desafío con Clostridium perfringens (C) sobre el crecimiento de pollos de engorde y la inducción de la infección por enteritis necrótica. Los resultados mostraron que la inoculación con Eimeria antes del desafío con Clostridium, aumentó en gran medida la severidad de la enteritis necrótica inducida en pollos de engorde, pero la adición de harina de pescado jugó sólo un papel marginal en el modelo de desafío. El rendimiento de las aves fue significativamente afectado por los tres factores durante el período experimental de 35 días. La harina de pescado aumentó el peso corporal, pero los efectos estadísticamente significativos de la harina de pescado no se observaron en la conversión alimenticia (FCR) y ni en el consumo de alimento. Tanto Eimeria y C. perfringens redujeron significativamente la ganancia de peso corporal y el consumo de alimento. La inoculación de Eimeria pero no la inoculación con C. perfringens indujo significativamente una pobre conversión alimenticia. Estos hallazgos indican que la harina de pescado en la dieta puede ser removida del modelo para permitir que los resultados de rendimiento de los pollitos desafiados sean equivalentes al rendimiento de los pollitos en el campo. En conclusión, el presente estudio demuestra que un modelo de desafío de enteritis necrótica sin harina de pescado es válido y elimina el sesgo en el rendimiento de las aves en el modelo introducido por la alimentación con dietas altas en la harina de pescado, lo que refina el modelo para facilitar el rendimiento de resultados más relevantes a nivel comercial.

Necrotic enteritis is an enteric disease of poultry resulting from infection by Clostridium perfringens with coinfection by Eimeria spp. constituting a major risk factor for disease pathogenesis. This study compared three commercial broiler chicken lines using an experimental model of necrotic enteritis. Day-old male Cobb, Ross, and Hubbard broilers were orally infected with viable C. perfringens and E. maxima and fed a high-protein diet to promote the development of experimental disease. Body weight loss, intestinal lesions, and serum antibody levels against α-toxin and necrotic enteritis B-like (NetB) toxin were measured as parameters of disease susceptibility and host immune response. Cobb chickens exhibited increased body weight loss compared with Ross and Hubbard breeds and greater gut lesion severity compared with Ross chickens. NetB antibody levels were greater in Cobb chickens compared with the Ross or Hubbard groups. These results suggest that Cobb chickens may be more susceptible to necrotic enteritis in the field compared with the Ross and Hubbard lines. Nota de Investigación—Susceptibilidad relativa a la enfermedad y respuesta de anticuerpos contra toxinas clostridiales en tres líneas de pollo de engorde comerciales coinfectadas por Clostridium perfringens y Eimeria maxima utilizando un modelo experimental de enteritis necrótica. La enteritis necrótica es una enfermedad entérica de las aves comerciales que resulta de la coinfección por Clostridium perfringens y Eimeria spp. que constituye un factor de riesgo importante para la patogénesis de la enfermedad. En este estudio se compararon tres líneas de pollos de engorde comerciales utilizando un modelo experimental de enteritis necrótica. Pollos de engorde de un día de edad, de las líneas Cobb, Ross y Hubbard fueron infectados oralmente con C. perfringens y con E. maxima viables y fueron alimentados con una dieta alta en proteínas para favorecer el desarrollo de la enfermedad experimental. Se midieron la pérdida de peso corporal, las lesiones intestinales, y los niveles séricos de anticuerpos contra la toxina α y contra la toxina de enteritis necrótica similar a la toxina B (NetB) y se analizaron como parámetros de susceptibilidad a la enfermedad, también se midió la respuesta inmune del huésped. Los pollos de la línea Cobb mostraron una mayor pérdida de peso corporal en comparación con los pollos de las líneas Ross y Hubbard y mayor severidad de lesiones intestinales en comparación con los pollos Ross. Los niveles de anticuerpos contra la toxina NetB fueron mayores en pollos Cobb en comparación con los pollos de las líneas Ross y Hubbard. Estos resultados sugieren que los pollos Cobb pueden ser más susceptibles a la enteritis necrótica en el campo en comparación con las líneas Hubbard y Ross.

Gastrointestinal infection is often associated with hypophagia and weight loss; however, the precise mechanisms governing these responses remain poorly defined. Furthermore, the possibility that alterations in feeding during infection may be beneficial to the host requires further study. We used the nematode Trichinella spiralis, which transiently inhabits the small intestine before migrating to skeletal muscle, as a biphasic model of infection to determine the cellular and molecular pathways controlling feeding during enteric and peripheral inflammation. Through the infection of genetically modified mice lacking cholecystokinin, Tumor necrosis factor α receptors and T and B-cells, we observed a biphasic hypophagic response to infection resulting from two separate immune-driven mechanisms. The enteroendocrine I-cell derived hormone cholecystokinin is an essential mediator of initial hypophagia and is induced by CD4+ T-cells during enteritis. In contrast, the second hypophagic response is extra-intestinal and due to the anorectic effects of TNFα during peripheral infection of the muscle. Moreover, via maintaining naive levels of the adipose secreted hormone leptin throughout infection we demonstrate a novel feedback loop in the immunoendocrine axis. Immune driven I-cell hyperplasia and resultant weight loss leads to a reduction in the inflammatory adipokine leptin, which in turn heightens protective immunity during infection. These results characterize specific immune mediated mechanisms which reduce feeding during intestinal or peripheral inflammation. Importantly, the molecular mediators of each phase are entirely separate. The data also introduce the first evidence that I-cell hyperplasia is an adaptively driven immune response that directly impinges on the outcome to infection.

Upper gastrointestinal endoscopy showed characteristic findings of gastro-oesophageal reflux disease and Barrett's oesophagus (confirmed by pathological study); an isolated, thickened gastric fold (which was biopsied; figure); and no macroscopic evidence of erythema, oedema, erosive gastritis, ulcerations, tumour-like nodules, or worms.

The pathologic, molecular, and immunohistochemical findings associated with Neorickettsia helminthoeca are described in coatis (Nasua nasua). Tissue sections (small intestine, lungs, kidney, liver, and spleen) of coatis (n = 3) that died at the Bela Vista Biological Refuge, Foz do Iguaçu, Paraná, southern Brazil were routinely processed from histopathology. Selected formalin-fixed paraffin-embedded (FFPE) tissue sections of the small intestine, lungs, and spleen were used in an immunohistochemical (IHC) assay designed to identify the antigens of N. helminthoeca. Additionally, FFPE tissue sections of the small intestine were used to demonstrate antigens of canine parvovirus-2 (CPV-2) by IHC. Histopathology revealed chronic enteritis in all coatis. Parasitic enteritis was diagnosed in two coatis; one of these contained examples of a trematode within the lumen of the small intestine and the ovum of a trematode encysted in the intestinal mucosa. Other significant pathologic findings included interstitial pneumonia (n = 2) and pyogranulomatous splenitis (n = 1). Positive immunolabeling for N. helminthoeca was identified within macrophages of the small intestine and reticuloendothelial cells within the germinal centers of the spleen of all coatis; the intestinal trematode was N. helminthoeca IHC-positive. All pulmonary sections revealed negative immunolabeling for N. helminthoeca. Furthermore, the antigens of CPV-2 were not identified in the intestine of any coati. These findings indicate that these coatis were infected by N. helminthoeca, but since clinical and gross pathological findings were not recorded, it is uncertain if this pathogen produced clinical disease in this canid host; therefore, coatis may be asymptomatic or dead-end hosts for this organism.

Necrotic enteritis (NE) in poultry is the most important bacterial disease in terms of economic losses. The present study was conducted to evaluate the effect of an experimental challenge with necrotic enteritis on respiration and heat production in birds pretreated with dietary acylated starch or antibiotics (AB) zinc bacitracin (50 mg/kg) plus salinomycin (60 mg/kg). In total, 48 1-day-old Ross 308 male broilers were assigned to floor pens until day 10. On day 11, birds were randomly placed into 16 calorimetric chambers with four replicates of three birds per treatment. Treatments were: control, AB, acetylated high-amylose maize starch (SA), or butyrylated high-amylose maize starch (SB). Birds were NE challenged by inoculation with 5000 sporulated oocysts each of Eimeria maxima and Eimeria acervulina and 2500 sporulated oocysts of Eimeria brunetti on day 9 and Clostridium perfringens (3.8 × 108 colony-forming units) on day 14. The results showed that heat production (HP), respiratory quotient (RQ), heat increment, weight gain (WG), feed intake (FI), and livability (LV) of birds fed control, SA, and SB diets were lower than birds fed AB at 19 and 42 hr postinoculation (P < 0.05). At 65 hr postchallenge, increased FI and WG of birds were observed, indicating recovery from NE. During the entire period, from day 14 to day 17, birds fed control, SA, and SB had lower WG, FI, HP, RQ, metabolizable energy intake (MEI), and metabolizable energy (P < 0.01) than those fed AB. The data demonstrate that Eimeria sp. and C. perfringens challenge reduces growth performance, HP, RQ, metabolizable energy, and MEI of birds fed control, SA, and SB but not AB diets.

Over 4 years, only two known cases of fluke invasions were diagnosed in racing pigeons (Columba livia) originating from different regions of Poland. In both cases, the invasion was characterized by a very high mortality (approximately 70%), and the source of the infestation was snails of the Lymnaeidae family eaten by pigeons. Fluke invasions in pigeons are extremely rare and to date have not been described in Poland. Therefore, the occurrence of the symptoms of hemorrhagic diarrhea and sudden deaths of either adult pigeons or nestlings were suspected to be associated with poisoning. Autopsy revealed an invasion of flukes causing hemorrhagic enteritis. Renal failure and spleen atrophy were also found in the birds. Using molecular biology techniques, infestation with the fluke Echinostoma revolutum was determined in the second case.