Aquatic bird bornavirus (ABBV-1), an avian bornavirus, has been reported in wild waterfowl from North America and Europe that presented with neurological signs and inflammation of the central and peripheral nervous systems. The potential of ABBV-1to infect and cause lesions in commercial waterfowl species is unknown. The aim of this study was to determine the ability of ABBV-1 to infect and cause disease in day-old Muscovy ducks (n = 174), selected as a representative domestic waterfowl. Ducklings became infected with ABBV-1 through both intracranial and intramuscular, but not oral, infection routes. Upon intramuscular infection, the virus spread centripetally to the central nervous system (brain and spinal cord), while intracranial infection led to virus spread to the spinal cord, kidneys, proventriculus, and gonads (centrifugal spread). Infected birds developed both encephalitis and myelitis by 4 weeks post infection (wpi), which progressively subsided by 8 and 12 wpi. Despite development of microscopic lesions, clinical signs were not observed. Only five birds had choanal and/or cloacal swabs positive for ABBV-1, suggesting a low potential of Muscovy ducks to shed the virus. This is the first study to document the pathogenesis of ABBV-1 in poultry species, and confirms the ability of ABBV-1 to infect commercial waterfowl.
In Ontario, within the past few years, there has been a marked increase in the number of non-commercial poultry flocks (referred to as "small flocks"). Small poultry flocks may act as a reservoir of avian and zoonotic pathogens, given the flocks' limited access to veterinary services, inadequate biosecurity practices, and increased risk of contact with wild birds. Despite these potential risks, there is a scarcity of data concerning the prevalence of poultry and zoonotic pathogens among these flocks. To assess the baseline prevalence of bacterial and viral infectious pathogens, prospective surveillance of small flock postmortem submissions to the Animal Health Laboratory was conducted over a 2-y period. With the owner's consent, a postmortem examination and pre-set tests for infectious agents were conducted. A total of 160 submissions, mainly chickens (84%), were received. Among bacterial pathogens, Brachyspira spp., Mycoplasma synoviae, Campylobacter spp., Mycoplasma gallisepticum, and Salmonella spp. were detected in 37%, 36%, 35%, 23%, and 3% of tested submissions, respectively. Among viral pathogens, infectious bronchitis virus, fowl adenovirus, infectious laryngotracheitis virus, avian reovirus, and infectious bursal disease virus were detected in 39%, 35%, 15%, 4%, and 1% of submissions, respectively. We detected non-virulent avian avulavirus 1 from two chickens in a single submission, and low-pathogenic H10N8 influenza A virus from a single turkey submission. Our study provides baseline prevalence of viral and bacterial pathogens circulating in Ontario small flocks and may help animal and human health professionals to educate small flock owners about disease prevention.
Ophidiomycosis (snake fungal disease) is caused by the fungus Ophidiomyces ophiodiicola. As ophidiomycosis is difficult to study in free-ranging snakes, a reliable experimental model is needed to investigate transmission, pathogenesis, morbidity, and mortality, and the effects of brumation and temperature on disease development. Our objective was to develop such a model via subcutaneous injection of O. ophiodiicola conidia in red cornsnakes ( Pantherophis guttatus). The model was used to evaluate transmission and the effects of brumation and temperature in co-housed inoculated and noninoculated snakes. All 23 inoculated snakes developed lesions consistent with ophidiomycosis, including heterophilic and granulomatous dermatitis, cellulitis, and myositis, and embolic fungal granulomas throughout the liver and the coelomic connective tissue in 21/23 (91%). In the inoculated snakes, 21% of skin swabs, 37% of exuvia, and all liver samples tested positive by qPCR (quantitative polymerase chain reaction) for O. ophiodiicola. A post brumation skin swab from 1/12 noninoculated snakes that brumated in contact with inoculated snakes tested positive by qPCR, suggesting possible contact transmission. That snake had microscopic skin lesions consistent with ophidiomycosis, but no visible fungal elements. Of the 23 inoculated snakes, 20 (87%) died over the 70-day experiment, with ophidiomycosis considered the primary cause of death; 12 (52%) of the inoculated snakes died during brumation. Overall, this experimental model of ophidiomycosis reproduced skin lesions analogous to those of many natural cases, and internal lesions similar to the most severe natural cases. The study provides tentative experimental evidence for horizontal transmission in brumation, and offers a tool for future studies of this widespread snake disease.
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