Abstract
Escherichia coli constitutes an immense challenge to the poultry industry due to its devastating effect on productivity, mortality, and carcass condemnations. To aid future studies on disease mechanisms and interventions, an aerogenous infection model was established in adult broiler breeders. Hens (n = 120) were randomly allocated into six groups receiving either aerosolised E. coli or vehicle, or intratracheal E. coli or vehicle. Replication of aerosol inoculation was performed on distinct days. Alternating euthanasia time points were predetermined in order to evaluate the progression of the disease. All animals were thoroughly necropsied, and bacteriological samples were collected as well as tissues for histopathology. Birds inoculated with E. coli exhibited clinical signs and developed characteristic gross and histopathological lesions of colibacillosis, including splenic fibrinoid necrosis, folliculitis, polyserositis and impaction of parabronchi with fibrinoheterophilic exudate and necrotic debris, as well as positive in situ localisation of intralesional E. coli by immunohistochemistry. This study presents a successful development of a discriminative colibacillosis model through aerosol inoculation of adult broiler breeders. Gross and histopathological lesions characteristic of colibacillosis were established in two independent experiments.
Highlights
Abbreviations AE Avian encephalomyelitis BA Blood agar BW Bodyweight CAV Chicken anaemia virus colony forming units (CFU) Colony-forming unit d Day dpi Days post-infection E. coli Escherichia coli IB Infectious bronchitis virus IBD Infectious bursal disease LB Lysogeny broth IT Intratracheal n Number optical density (OD) Optical density W Week of life
The lesions inflicted by E. coli in poultry are typically extraintestinal, often collectively referred to as colibacillosis and manifest in a number of ways including cellulitis, omphalitis and yolksacculitis, peritonitis, perihepatitis, pericarditis, airsacculitis, oophoritis, salpingitis, arthritis and o steomyelitis[1,10]
The pathogenesis of avian colibacillosis is often attributed to the respiratory route[10,14], with ascending infections via the oviduct, entrance through a compromised skin barrier and translocation of bacteria from the intestinal tract as additional important routes of infection[15,16,17]
Summary
Abbreviations AE Avian encephalomyelitis BA Blood agar BW Bodyweight CAV Chicken anaemia virus CFU Colony-forming unit d Day dpi Days post-infection E. coli Escherichia coli IB Infectious bronchitis virus IBD Infectious bursal disease LB Lysogeny broth IT Intratracheal n Number OD Optical density W Week of life. As a natural inhabitant of the intestinal tract, E. coli is continuously passed to the environment through droppings[10,11] providing a potential source for dissemination through dust within housing facilities with numbers as high as 1 06 colony forming units (CFU) per gram being r eported[12]. A wide range of models attempting to mimic colibacillosis in controlled settings has been developed in domestic poultry with varying degrees of success and invasiveness, e.g., inoculation intratracheally, directly into air sacs, intra-uterine, subcutaneously, intravenously, as well as through aerosols in layers and small chickens, and intraperitoneally[14,15,16,18,19,20,21]
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