YERSINIA PSEUDOTUBERCULOSIS, SEROGROUP O:1A, INFECTION IN TWO AMAZON PARROTS (AMAZONA AESTIVA AND AMAZONA ORATRIX) WITH HEPATIC HEMOSIDEROSIS.

Necropsies were conducted on a female blue-fronted Amazon (Amazona aestiva) and a female yellow-headed Amazon (Amazona oratrix) that died after depression, ruffled feathers, diarrhea, and biliverdin in the urine. Gross and microscopic examinations revealed multifocal necrosis in the liver, spleen, lungs, kidneys, intestines, and heart caused by acute bacteremia. Yersinia pseudotuberculosis, serogroup O:1a, was isolated by culturing from the visceral lesions in the liver, intestines, and spleen. Virulence gene analysis showed the presence of the inv gene and the complete pathogenicity island: IS100, psn, yptE, irp1, irp2 ybtP-ybtQ, ybtX-ybtS, and int asnT-Int. Histopathologic findings and chemical analysis also demonstrated hepatic hemosiderosis. As has been demonstrated in other species, hemosiderosis may predispose Amazona spp. to systemic infection with Y. pseudotuberculosis after enteric disease.

Infectious bronchitis corona virus establishes productive infection in avian macrophages interfering with selected antimicrobial functions.

Infectious bronchitis virus (IBV) causes respiratory disease leading to loss of egg and meat production in chickens. Although it is known that macrophage numbers are elevated in the respiratory tract of IBV infected chickens, the role played by macrophages in IBV infection, particularly as a target cell for viral replication, is unknown. In this study, first, we investigated the ability of IBV to establish productive replication in macrophages in lungs and trachea in vivo and in macrophage cell cultures in vitro using two pathogenic IBV strains. Using a double immunofluorescent technique, we observed that both IBV Massachusetts-type 41 (M41) and Connecticut A5968 (Conn A5968) strains replicate in avian macrophages at a low level in vivo. This in vivo observation was substantiated by demonstrating IBV antigens in macrophages following in vitro IBV infection. Further, IBV productive infection in macrophages was confirmed by demonstrating corona viral particles in macrophages and IBV ribonucleic acid (RNA) in culture supernatants. Evaluation of the functions of macrophages following infection of macrophages with IBV M41 and Conn A5968 strains revealed that the production of antimicrobial molecule, nitric oxide (NO) is inhibited. It was also noted that replication of IBV M41 and Conn A5968 strains in macrophages does not interfere with the induction of type 1 IFN activity by macrophages. In conclusion, both M41 and Con A5968 IBV strains infect macrophages in vivo and in vitro resulting productive replications. During the replication of IBV in macrophages, their ability to produce NO can be affected without affecting the ability to induce type 1 IFN activity. Further studies are warranted to uncover the significance of macrophage infection of IBV in the pathogenesis of IBV infection in chickens.

Modelling the Northward Expansion of Culicoides sonorensis (Diptera: Ceratopogonidae) under Future Climate Scenarios.

Climate change is affecting the distribution of pathogens and their arthropod vectors worldwide, particularly at northern latitudes. The distribution of Culicoides sonorensis (Diptera: Ceratopogonidae) plays a key role in affecting the emergence and spread of significant vector borne diseases such as Bluetongue (BT) and Epizootic Hemorrhagic Disease (EHD) at the border between USA and Canada. We used 50 presence points for C. sonorensis collected in Montana (USA) and south-central Alberta (Canada) between 2002 and 2012, together with monthly climatic and environmental predictors to develop a series of alternative maximum entropy distribution models. The best distribution model under current climatic conditions was selected through the Akaike Information Criterion, and included four predictors: Vapour Pressure Deficit of July, standard deviation of Elevation, Land Cover and mean Precipitation of May. This model was then projected into three climate change scenarios adopted by the IPCC in its 5th assessment report and defined as Representative Concentration Pathways (RCP) 2.6, 4.5 and 8.5. Climate change data for each predictor and each RCP were calculated for two time points pooling decadal data around each one of them: 2030 (2021-2040) and 2050 (2041-2060). Our projections showed that the areas predicted to be at moderate-high probability of C. sonorensis occurrence would increase from the baseline scenario to 2030 and from 2030 to 2050 for each RCP. The projection also indicated that the current northern limit of C. sonorensis distribution is expected to move northwards to above 53°N. This may indicate an increased risk of Culicoides-borne diseases occurrence over the next decades, particularly at the USA-Canada border, as a result of changes which favor C. sonorensis presence when associated to other factors (i.e. host and pathogen factors). Recent observations of EHD outbreaks in northern Montana and southern Alberta supported our projections and considerations. The results of this study can inform the development of cost effective surveillance programs, targeting areas within the predicted limits of C. sonorensis geographical occurrence under current and future climatic conditions.

Induction of innate immune response following infectious bronchitis corona virus infection in the respiratory tract of chickens.

Infectious bronchitis virus (IBV) replicates in the epithelial cells of trachea and lungs of chicken, however the mechanism of generation of innate immune response against IBV infection in these tissues has not been fully characterized. Our objective was to study innate responses induced early following IBV infection in chickens. Initiation of the transcription of selected innate immune genes such as TLR3, TLR7, MyD88, IL-1ß and IFN-ß, as well as recruitment of macrophages, were evident following an initial down regulation of some of the observed genes (TLR3, IL-1ß, and IFN-γ) in trachea and lung. This initial down-regulation followed by the induction of innate immune response to IBV infection appears to be inadequate for the control of IBV genome accumulation and consequent histopathological changes in these tissues. Potential induction of innate immunity before infection occurs may be necessary to reduce the consequences since vaccine induced immunity is slow to develop.