13 research outputs found

    The pathogenesis of colibacillosis in broilers infected with virulent or vaccine strains of infectious bronchitis virus

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    Colibacillosis is caused by E. coli bacteria and occurs predominantly in broilers in the second half of the growing period. The disease is of economic importance worldwide due to growth retardation, increased feed conversion, mortality and high condemnation rate at slaughter. Moreover, colibacillosis results in impaired welfare. Infections of the respiratory tract, amongst others infection with infectious bronchitis virus (IBV), increase the susceptibility for colibacillosis of broilers significantly. From recently made field observations it was hypothesised that not only virulent IBV but also live IBV vaccine strains, which are commonly used in the field to prevent birds from clinical signs of infectious bronchitis (IB), are able to increase colibacillosis susceptibility in broilers substantially. This hypothesis was tested experimentally. The experiments showed that IBV vaccines H120 and H52 increased colibacillosis susceptibility in four-weeks-old broilers to the same level as virulent IBV strains (M41 and D387) did. It was also demonstrated that the IBV H120 vaccine spread extensively between broilers. From the latter data it seems obvious that IBV H120 vaccine also might spread between flocks. In case not IB vaccinated flocks are infected with IB vaccine virus by that route, especially in the second half of the growing period, serious colibacillosis might occur. The significance of IBV vaccine strains in the occurrence of colibacillosis in broilers in the field has to be elucidated. The underlying mechanism of E. coli superinfections (E. coli infection after triggering by a previous viral infection) in IBV infected broilers was studied based on morphological and functional immunology. The results strongly suggest that preceding infection with vaccine or virulent IBV does not seem to impair the clearance of the E. coli in the respiratory tract of broilers, but rather induces an exaggerated inflammatory response. It also seems that infection with virulent or vaccine strains of IBV altered the innate systemical immunity rather than the phagocytic cell function

    Transmissibility of Infectious Bronchitis Virus H120 Vaccine Strain Among Broilers under Experimental Conditions

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    The aim of this study was to quantify transmission of infectious bronchitis virus (IBV) H120 vaccine strain among broilers, and to assess whether birds that have been exposed to vaccine strain-shedding birds were protected against clinical signs after infection with a virulent strain of the same serotype. A transmission experiment and a replicate were carried out, each with six groups of commercial broilers. At day of hatch (n 5 30) or at 15 days of age (n 5 20), half of each group was inoculated with either IBV H120 vaccine (H120 group), virulent IBV M41 (M41 group), or were mock-infected, thereby contact-exposing the other half of each group. Nasal discharge was recorded, and antibody response and virus shedding were measured. To measure clinical protection, four weeks after inoculation all birds, in all groups, were challenged with IBV M41. The reproduction ratio (R; the average number of contact infections caused by one infectious bird) was determined to quantify virus transmission. All contactexposed birds, except for one in an H120 group, became infected with either IBV H120 or IBV M41. Almost all birds contactinfected with IBV H120 or IBV M41 were subsequently protected against clinical signs after challenge with IBV M41. The lower limits of the 95% confidence interval (CI) of the R of IBV H120 vaccine, and of IBV M41, were significantly ,1. For both IBV H120 and IBV M41, the 95% CI was [2.1–‘] following inoculation at day of hatch and [1.8–‘] after inoculation at 15 days of age. This finding demonstrates that IBV H120 vaccine is able to spread extensively among broilers. This implies that this vaccine strain might be able to become endemically present in the poultry population. It also implies that, even if not all birds received vaccine during spray application, due to the ability of the vaccine to spread in the flock, they will most likely be protected against clinical signs after a subsequent field virus infection

    Transmissibility of Infectious Bronchitis Virus H120 Vaccine Strain Among Broilers under Experimental Conditions

    No full text
    The aim of this study was to quantify transmission of infectious bronchitis virus (IBV) H120 vaccine strain among broilers, and to assess whether birds that have been exposed to vaccine strain-shedding birds were protected against clinical signs after infection with a virulent strain of the same serotype. A transmission experiment and a replicate were carried out, each with six groups of commercial broilers. At day of hatch (n 5 30) or at 15 days of age (n 5 20), half of each group was inoculated with either IBV H120 vaccine (H120 group), virulent IBV M41 (M41 group), or were mock-infected, thereby contact-exposing the other half of each group. Nasal discharge was recorded, and antibody response and virus shedding were measured. To measure clinical protection, four weeks after inoculation all birds, in all groups, were challenged with IBV M41. The reproduction ratio (R; the average number of contact infections caused by one infectious bird) was determined to quantify virus transmission. All contactexposed birds, except for one in an H120 group, became infected with either IBV H120 or IBV M41. Almost all birds contactinfected with IBV H120 or IBV M41 were subsequently protected against clinical signs after challenge with IBV M41. The lower limits of the 95% confidence interval (CI) of the R of IBV H120 vaccine, and of IBV M41, were significantly ,1. For both IBV H120 and IBV M41, the 95% CI was [2.1–‘] following inoculation at day of hatch and [1.8–‘] after inoculation at 15 days of age. This finding demonstrates that IBV H120 vaccine is able to spread extensively among broilers. This implies that this vaccine strain might be able to become endemically present in the poultry population. It also implies that, even if not all birds received vaccine during spray application, due to the ability of the vaccine to spread in the flock, they will most likely be protected against clinical signs after a subsequent field virus infection

    Rapid NK-cell activation in chicken after infection with infectious bronchitis virus M41

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    Natural killer (NK) cells are cytotoxic lymphocytes and play an important role in the early defence against viruses. In this study we focussed on NK cell and interferon (IFN) responses after infection with infectious bronchitis virus (IBV). Based on surface expression of CD107+, enhanced activation of lung NK cells was observed at 1. dpi, whereas in blood prolonged NK-cell activation was found. IFN-α and IFN-β mRNA and proteins were not rapidly induced whereas IFN-γ production in lung, measured by Elispot assay, increased over time at 2 and 4. dpi. In contrast, IFN-γ production in blood was highest at 1. dpi and decreased over time down to levels comparable to uninfected birds at 4. dpi. Collectively, infection with IBV-M41 resulted in activation of NK cells in the lung and blood and rapid production of IFN-γ and not IFN-α and IFN-β compared to uninfected birds

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    No full text
    Natural killer (NK) cells are cytotoxic lymphocytes and play an important role in the early defence against viruses. In this study we focussed on NK cell and interferon (IFN) responses after infection with infectious bronchitis virus (IBV). Based on surface expression of CD107+, enhanced activation of lung NK cells was observed at 1 dpi, whereas in blood prolonged NKcell activation was found. IFN- and IFN- mRNA and proteins were not rapidly induced whereas IFN- production in lung, measured by Elispot assay, increased over time at 2 and 4 dpi. In contrast, IFN- production in blood was highest at 1 dpi and decreased over time down to levels comparable to uninfected birds at 4 dpi. Collectively, infection with IBV-M41 resulted in activation of NK cells in the lung and blood and rapid production of IFN- and not IFN- and IFN- compared to uninfected birds

    Outbreak of avian influenza H7N3 on a turkey farm in the Netherlands

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    This case report describes the course of an outbreak of avian influenza on a Dutch turkey farm. When clinical signs were observed their cause remained unclear. However, serum samples taken for the monitoring campaign launched during the epidemic of highly pathogenic avian influenza in 2003, showed that all the remaining turkeys were seropositive against an H7 strain of avian influenza virus, and the virus was subsequently isolated from stored carcases. The results of a reverse-transcriptase PCR showed that a H7N3 strain was involved, and it was characterised as of low pathogenicity. However, its intravenous pathogenicity index was 2.4, characterising it as of high pathogenicity, suggesting that a mixture of strains of low and high pathogenicity may have been present in the isolate. The outbreak remained limited to three farms

    Selective breeding for high natural antibody level increases resistance to avian pathogenic Escherichia coli (APEC) in chickens

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    Keyhole limpet hemocyanin (KLH)-binding natural antibody (NAb) titers in chickens are heritable, and higher levels have previously been associated with a higher survival. This suggests that selective breeding for higher NAb levels might increase survival by means of improved general disease resistance. Chickens were divergently selected and bred for total NAb levels binding KLH at 16 weeks of age for six generations, resulting in a High NAb selection line and a Low NAb selection line. To for test differences in disease resistance, chickens were challenged with avian pathogenic Escherichia coli (APEC) in two separate experiments. Chickens at 8 days of age received one of four intratracheal inoculations of 0.2 mL phosphate buffered saline (PBS): 1) mock inoculate, 2) with 0.2 mL PBS containing 108.20 colony-forming units (CFU)/mL APEC, 3) with 0.2 mL PBS containing 106.64 CFU/mL APEC, and 4) with 0.2 mL PBS containing 107.55 CFU/mL APEC. Mortality was recorded during 7 days post inoculation. Overall, 50–60% reduced mortality was observed in the High line compared to the Low line for all APEC doses. In addition, morbidity was determined of the surviving chickens at 15 days of age. The High line had lower morbidity scores compared to the Low line. We conclude that selective breeding for high KLH-binding NAb levels at 16 weeks of age increase APEC resistance in early life. This study and previous studies support the hypothesis that KLH-binding NAb might be used as an indicator trait for to selective breed for general disease resistance in an antigen non-specific fashion.</p

    Broiler resilience to colibacillosis is affected by incubation temperature and post-hatch feeding strategy

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    Colibacillosis is a poultry disease that negatively affects welfare and causes economic losses. Treatment with antibiotics raises concerns on antimicrobial resistance. Consequently, alternative approaches to enhance poultry resilience are needed. Access to feed and water directly after hatch (early feeding) may enhance resilience at later ages. Additionally, a high eggshell temperature (EST) during mid incubation may improve chick quality at hatch, supporting potential positive effects of early feeding. Effects of EST [37.8°C (control) or 38.9°C (higher)] during mid-incubation (embryo days 7–14) and feeding strategy (early feeding or 48 h delayed feeding) were tested in a 2 × 2 factorial arrangement. At hatch, ̴ 1,800 broilers were divided over 36 pens and grown for 6 wk. At d 8 post hatch, avian pathogenic E. coli (APEC) was inoculated intratracheally as model to investigate broiler resilience against respiratory diseases. Incidence and severity of colibacillosis, local infection, and systemic infection were assessed at 6 moments between 3 h and 7 d postinoculation. Broilers were weighed daily during 13 d postinoculation and weekly thereafter. At higher EST, early feeding resulted in higher incidence of systemic infection compared to delayed feeding whereas at control EST, systemic infection was not different between feeding strategies. Regardless of EST, early compared to delayed feeding resulted in lower incidence of local infection, fewer BW deviations, and higher growth until d 35. In conclusion, early feeding could be considered as a strategy to enhance broiler resilience, but only when EST is not too high
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