Nahed A El-Shall, Mahmoud E Sedeik, Heba M Ismail, Ashraf M Awad
{"title":"鸡的实验性柔嫩艾美耳球虫感染后的极强感染性法氏囊病病毒攻击：临床和病理效果。","authors":"Nahed A El-Shall, Mahmoud E Sedeik, Heba M Ismail, Ashraf M Awad","doi":"10.1080/03079457.2025.2547583","DOIUrl":null,"url":null,"abstract":"<p><p>Infectious bursal disease (IBD) is an immunosuppressive disease that increases susceptibility to avian coccidiosis, but the contrary is unclear. In a battery trial, this study evaluated whether prior <i>E. tenella</i> (ET) infection of Egyptian Baladi chickens increased the virulence of the very virulent IBD virus. Birds grouped as follows: G1 (control), G2 (ET, 1.5×10<sup>4</sup> oocysts), G3 (ET, 5×10<sup>4</sup> oocysts), G4 (IBDV), G5 (G2+BDV), and G6 (G3+IBDV). At 21 days of age (d), chickens were sham- (G1 and 4) or ET- (G2, 3, 5, and 6) challenged. Four days later, G4-6 received IBDV by intranasal/ocular route. The birds were evaluated for growth performance and inspected clinically. The phagocytic test, cloacal viral shedding, and immunological organ index were evaluated on days 28 and 32. On day 28, the bursa of Fabricius (BF), spleen, and caecum were histologically analyzed, and caecal lesions were scored macroscopically. Compared to the G1, all challenged groups displayed worse growth performance (<i>P</i> ≤ 0.01). G5 and 6 outperformed G4 regarding weight gain and FI (P≤0.01), however, they still lagged behind G2 and 3 (<i>P</i> ≤ 0.01). Interestingly, the BF of G2 and 3 had a higher mean severity index (MSI) than G1 (<i>P</i> ≤ 0.01), indicating histological evidence of Eimeria stages. Nonetheless, G4's MSI was higher than G2's and G3's (<i>P</i> ≤ 0.01). Compared to G4, G5 and G6 displayed a substantially lower MSI and a higher BF' index. Mortalities in G4 and G6 were 10% and 5%, respectively. Compared to G4, G5 and 6 displayed increased viral shedding titers (<i>P</i> ≤ 0.01). Regarding coccidiosis, G5 and G6 exhibited lower phagocytic activity and higher oocyst counts and caecal lesion scores than G2 and G3 (<i>P</i> ≤ 0.01), suggesting that exposure to IBDV after ET enhanced ET pathogenicity and reproduction. Conclusions: ET interfered with the IBDV pathogenesis (increase in viral shedding, but less severe lesions compared to mono-infected birds); this could be because prior ET infection modulated T cells.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"1-12"},"PeriodicalIF":2.2000,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Experimental <i>Eimeria tenella</i> infection of chickens followed by very virulent infectious bursal disease viral challenge: clinical and pathological effects.\",\"authors\":\"Nahed A El-Shall, Mahmoud E Sedeik, Heba M Ismail, Ashraf M Awad\",\"doi\":\"10.1080/03079457.2025.2547583\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Infectious bursal disease (IBD) is an immunosuppressive disease that increases susceptibility to avian coccidiosis, but the contrary is unclear. In a battery trial, this study evaluated whether prior <i>E. tenella</i> (ET) infection of Egyptian Baladi chickens increased the virulence of the very virulent IBD virus. Birds grouped as follows: G1 (control), G2 (ET, 1.5×10<sup>4</sup> oocysts), G3 (ET, 5×10<sup>4</sup> oocysts), G4 (IBDV), G5 (G2+BDV), and G6 (G3+IBDV). At 21 days of age (d), chickens were sham- (G1 and 4) or ET- (G2, 3, 5, and 6) challenged. Four days later, G4-6 received IBDV by intranasal/ocular route. The birds were evaluated for growth performance and inspected clinically. The phagocytic test, cloacal viral shedding, and immunological organ index were evaluated on days 28 and 32. On day 28, the bursa of Fabricius (BF), spleen, and caecum were histologically analyzed, and caecal lesions were scored macroscopically. Compared to the G1, all challenged groups displayed worse growth performance (<i>P</i> ≤ 0.01). G5 and 6 outperformed G4 regarding weight gain and FI (P≤0.01), however, they still lagged behind G2 and 3 (<i>P</i> ≤ 0.01). Interestingly, the BF of G2 and 3 had a higher mean severity index (MSI) than G1 (<i>P</i> ≤ 0.01), indicating histological evidence of Eimeria stages. Nonetheless, G4's MSI was higher than G2's and G3's (<i>P</i> ≤ 0.01). Compared to G4, G5 and G6 displayed a substantially lower MSI and a higher BF' index. Mortalities in G4 and G6 were 10% and 5%, respectively. Compared to G4, G5 and 6 displayed increased viral shedding titers (<i>P</i> ≤ 0.01). Regarding coccidiosis, G5 and G6 exhibited lower phagocytic activity and higher oocyst counts and caecal lesion scores than G2 and G3 (<i>P</i> ≤ 0.01), suggesting that exposure to IBDV after ET enhanced ET pathogenicity and reproduction. Conclusions: ET interfered with the IBDV pathogenesis (increase in viral shedding, but less severe lesions compared to mono-infected birds); this could be because prior ET infection modulated T cells.</p>\",\"PeriodicalId\":8788,\"journal\":{\"name\":\"Avian Pathology\",\"volume\":\" \",\"pages\":\"1-12\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2025-09-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Avian Pathology\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://doi.org/10.1080/03079457.2025.2547583\",\"RegionNum\":2,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"VETERINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Avian Pathology","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.1080/03079457.2025.2547583","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"VETERINARY SCIENCES","Score":null,"Total":0}
Experimental Eimeria tenella infection of chickens followed by very virulent infectious bursal disease viral challenge: clinical and pathological effects.
Infectious bursal disease (IBD) is an immunosuppressive disease that increases susceptibility to avian coccidiosis, but the contrary is unclear. In a battery trial, this study evaluated whether prior E. tenella (ET) infection of Egyptian Baladi chickens increased the virulence of the very virulent IBD virus. Birds grouped as follows: G1 (control), G2 (ET, 1.5×104 oocysts), G3 (ET, 5×104 oocysts), G4 (IBDV), G5 (G2+BDV), and G6 (G3+IBDV). At 21 days of age (d), chickens were sham- (G1 and 4) or ET- (G2, 3, 5, and 6) challenged. Four days later, G4-6 received IBDV by intranasal/ocular route. The birds were evaluated for growth performance and inspected clinically. The phagocytic test, cloacal viral shedding, and immunological organ index were evaluated on days 28 and 32. On day 28, the bursa of Fabricius (BF), spleen, and caecum were histologically analyzed, and caecal lesions were scored macroscopically. Compared to the G1, all challenged groups displayed worse growth performance (P ≤ 0.01). G5 and 6 outperformed G4 regarding weight gain and FI (P≤0.01), however, they still lagged behind G2 and 3 (P ≤ 0.01). Interestingly, the BF of G2 and 3 had a higher mean severity index (MSI) than G1 (P ≤ 0.01), indicating histological evidence of Eimeria stages. Nonetheless, G4's MSI was higher than G2's and G3's (P ≤ 0.01). Compared to G4, G5 and G6 displayed a substantially lower MSI and a higher BF' index. Mortalities in G4 and G6 were 10% and 5%, respectively. Compared to G4, G5 and 6 displayed increased viral shedding titers (P ≤ 0.01). Regarding coccidiosis, G5 and G6 exhibited lower phagocytic activity and higher oocyst counts and caecal lesion scores than G2 and G3 (P ≤ 0.01), suggesting that exposure to IBDV after ET enhanced ET pathogenicity and reproduction. Conclusions: ET interfered with the IBDV pathogenesis (increase in viral shedding, but less severe lesions compared to mono-infected birds); this could be because prior ET infection modulated T cells.
期刊介绍：
Avian Pathology is the official journal of the World Veterinary Poultry Association and, since its first publication in 1972, has been a leading international journal for poultry disease scientists. It publishes material relevant to the entire field of infectious and non-infectious diseases of poultry and other birds. Accepted manuscripts will contribute novel data of interest to an international readership and will add significantly to knowledge and understanding of diseases, old or new. Subject areas include pathology, diagnosis, detection and characterisation of pathogens, infections of possible zoonotic importance, epidemiology, innate and immune responses, vaccines, gene sequences, genetics in relation to disease and physiological and biochemical changes in response to disease. First and subsequent reports of well-recognized diseases within a country are not acceptable unless they also include substantial new information about the disease or pathogen. Manuscripts on wild or pet birds should describe disease or pathogens in a significant number of birds, recognizing/suggesting serious potential impact on that species or that the disease or pathogen is of demonstrable relevance to poultry. Manuscripts on food-borne microorganisms acquired during or after processing, and those that catalogue the occurrence or properties of microorganisms, are unlikely to be considered for publication in the absence of data linking them to avian disease.
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