Footpad dermatitis (FPD) is a condition that causes necrotic lesions on the plantar surface of the footpads in growing broilers and turkeys. This condition not only causes downgrades and condemnations of saleable chicken paws, the portion of the leg below the spur, but is also an animal welfare concern in both the United States and in Europe.. Revenue from chicken paws in 2008 alone was worth $280 million. Harvesting large, unblemished paws has become a priority to poultry companies all over the world. Research on this subject has been ongoing since the 1940s and has looked into many different areas including nutrition, environment, and genetics. Early research looked at nutritional deficiencies such as riboflavin and biotin mainly in turkey poults. This early research was most likely looking at a separate form of dermatitis than what is being investigated now. Recent findings have suggested that there is a myriad of interacting factors that lead to FPD. Litter moisture appears to be the most likely culprit in the onset of this condition. Research has also shown a possible genetic link in the susceptibility to development of FPD lesions. Current chicken paw prices have skyrocketed due to a large export market in Asia. To produce unblemished paws for both increased profit and comply with current animal welfare recommendations, further research is needed to understand how the condition develops and what strategies can be used to prevent it.
Low pathogenicity avian influenza virus (LPAIV) and lentogenic Newcastle disease virus (lNDV) are commonly reported causes of respiratory disease in poultry worldwide with similar clinical and pathobiological presentation. Co-infections do occur but are not easily detected, and the impact of co-infections on pathobiology is unknown. In this study chickens and turkeys were infected with a lNDV vaccine strain (LaSota) and a H7N2 LPAIV (A/turkey/VA/SEP-67/2002) simultaneously or sequentially three days apart. No clinical signs were observed in chickens co-infected with the lNDV and LPAIV or in chickens infected with the viruses individually. However, the pattern of virus shed was different with co-infected chickens, which excreted lower titers of lNDV and LPAIV at 2 and 3 days post inoculation (dpi) and higher titers at subsequent time points. All turkeys inoculated with the LPAIV, whether or not they were exposed to lNDV, presented mild clinical signs. Co-infection effects were more pronounced in turkeys than in chickens with reduction in the number of birds shedding virus and in virus titers, especially when LPAIV was followed by lNDV. In conclusion, co-infection of chickens or turkeys with lNDV and LPAIV affected the replication dynamics of these viruses but did not affect clinical signs. The effect on virus replication was different depending on the species and on the time of infection. These results suggest that infection with a heterologous virus may result in temporary competition for cell receptors or competent cells for replication, most likely interferon-mediated, which decreases with time.
IMPORTANCEThe spread of H5 subtype highly pathogenic avian influenza (HPAI) viruses of the Gs/GD lineage by migratory waterfowl is a serious concern for animal and public health. H5 and H7 HPAI viruses are considered to be adapted to gallinaceous species (chickens, turkeys, quail, etc.) and less likely to infect and transmit in wild ducks. In order to understand why this is different with certain Gs/GD lineage H5 HPAI viruses, we compared the pathogenicity and transmission of several H5 and H7 HPAI viruses from previous poultry outbreaks to Gs/GD lineage H5 viruses, including H5N1 (clade 2.2), H5N8 and H5N2 (clade 2.3.4.4) viruses, in mallards as a representative wild duck species. Surprisingly, most HPAI viruses examined in this study replicated well and transmitted among mallards; however, the three Gs/GD lineage H5 HPAI viruses replicated to higher titers, which could explain the transmission of these viruses in susceptible wild duck populations.
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