Enterococcus cecorum: Changing clinical presentation in an emerging poultry pathogen
Animal Health Laboratory, University of Guelph, Guelph, ON
AHL Newsletter 2023;27(2):19.
Since 2002, pathogenic strains of E. cecorum have been identified in chickens, starting with outbreaks in Scotland and the Netherlands, then progressing to other countries including Canada, USA, Iran, and South Africa. Prior to 2002, E. cecorum was identified as a commensal in avian species (e.g., turkeys, Muscovy ducks, pigeons, canaries) and mammals such as horses, cattle, pigs, dogs, and cats; however, but identification of pathogenic strains has had a significant impact on broiler and broiler breeder health and production. While E. cecorum emerged as primarily causing bone lesions and lameness, recent outbreaks have manifested as septicemia at an earlier age.
E. cecorum infection causes two stages of disease. Initially, 2 to 3-week-old broilers can become infected but remain asymptomatic, or have clinical signs of depression (i.e., ruffled feathers, closed eyes). Bacterial sepsis can cause lesions of hepatitis, pericarditis and splenomegaly resulting in increased mortality. Subsequently, 5 to 6-week-old broilers / broiler breeders (or slightly older broiler breeders ~13 weeks old) develop lameness or bilateral paralysis where birds can be found sitting with their legs extended forward. Mortality is usually higher at this stage due to culling, dehydration and starvation.
On postmortem examination, joint lesions typified by synovitis and arthritis of the coxofemoral, stifle, and hock joints have accumulation of creamy yellow fluid and sometimes caseous material resulting in joint swelling. Spondylitis and osteomyelitis can be identified in the free thoracic vertebra (FTV), proximal femur, or proximal tibia. Lesions in the free thoracic vertebra and adjacent vertebral bodies develop into a dorsally-expansile inflammatory mass that causes spinal cord compression resulting in bilateral paralysis. In severe cases, this vertebral mass expands ventrally into the celomic cavity and creates a localized enlargement of the spinal column that can be seen in the area of the caudal lungs / cranial kidneys.
E. cecorum lesions are similar to those caused by other infectious agents; therefore, bacterial culture is required to confirm the causative agent. It is possible to culture E. cecorum from the FTV and femoral heads without observing gross lesions. Commensal and pathogenic strains co-exist, and virulence varies among pathogenic strains. In multiple studies, it was found that commensal isolates have higher diversity whereas pathogenic isolates originating from different countries group phylogenetically. These belong predominantly to one clade, and are distinct from the commensal poultry isolates. There are few virulence factors identified in both the commensal and pathogenic strains of E. cecorum.
Even after 2 decades, the pathogenesis and transmission of E. cecorum is still under investigation, not only in chickens, but also in other avian species. It is known that pathogenic strains colonize the intestines and spread rapidly through a flock. It is also known that Enterococcus spp. (including E. cecorum) survive well in the environment, and this could be the source of repeated infections within a barn. Research has shown that E. cecorum survives longer in litter than in dust or on PVC material, and that there is longer survival at lower temperatures and at lower relative humidity. Pathogenic strains showed a longer survival time than commensals under similar conditions.
Currently, our understanding of E. cecorum is still evolving in avian species. Further research into transmission and sources of infection will aid in developing prevention and management strategies. AHL
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