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Spondylitis (vertebral Osteomyelitis)

Other Names: Vertebral Osteoarthritis

Spondylitis (vertebral osteomyelitis) is a form of bacterial chondronecrosis with osteomyelitis which affects the chicken's spinal cord. Fibronecrotic fibriscess develop in the free thoracic vertebra (FTV, the sixth thoracic vertebra) or in adjacent vertebrae.

It occurs when opportunistic bacteria are deposited through the bloodstream to the damaged vertebrae. Progressive necrosis and fibriscess formation occur, leading to enlargement of the vertebrae which compresses the spinal cord. This action results in demyelination and necrosis of the nervous tissue.

The most common bacteria isolated from the spinal fibriscesses are Enterococcus cecorum and E. faecalis. Infection with Staphylococcus aureus and E. hirae occur less commonly.

Clinical Signs of Spondylitis in Chickens


Clinical signs observed in birds with spondylitis include lameness (proportional to the degree of pressure on the spinal cord). As the condition worsens the bird eventually assumes a sitting position with their legs stretched out in front of them and a characteristic kyphosis (kinky back) may be visible.

Clinical Signs

Lameness
Hock-sitting
Legs stretched out in front while sitting
Depression
Kinky back visible

Diagnosis

  • History
  • Clinical signs
  • Radiographs
  • Necropsy

Reported Cases

  • Case 1: Enterococcal spondylitis in a Chickens Enterococcus cecorum was isolated from spondylitis lesions in broilers from two flocks in North Carolina that were experiencing increased mortality. Affected birds showed paresis and paralysis, clinical signs characteristic of enterococcal spondylitis (ES). Affected birds rested on their hocks and caudal abdomens with legs extended forward and were unable to stand or walk. Necropsy examination of affected birds revealed firm to hard inflammatory masses involving the vertebral bodies at the level of the free thoracic vertebra that bulged dorsally and compressed the spinal cord. When opened, lesions contained pale, tan to yellow caseonecrotic material. Microscopically, necrosis and fibrinoheterophilic spondylitis with intralesional gram-positive bacteria were seen. Heavy growth of E. cecorum recovered from vertebral lesions confirmed the diagnosis of ES. To investigate possible sources of the organism for one of the flocks bacterial cultures were made from the environment, water lines, mice trapped on the farm, cecal/cloacal swabs from one of the parent broiler breeder flocks, egg residue, hatching eggs, and the hatchery environment. Except for cecal/cloacal swabs from the breeders, E. cecorum was not isolated from any of these samples. When compared phenotypically and genotypically, cecal/cloacal isolates of E. cecorum from the breeders differed from isolates from spondylitis lesions in the broilers. The source of E. cecorum for the broiler flocks was not determined, but vertical transmission appears unlikely. Ref

  • Case 2: Enterococcal-associated vertebral osteoarthritis in a Chickens An outbreak of enterococcal-associated vertebral osteoarthritis (EVOA) in male broiler breeders occurred in several flocks in South Africa. Male birds aged 4 and 9 weeks displayed the common presentation of lameness, paresis or complete paralysis. Autopsies of culled birds revealed masses on caudal thoracic vertebrae T5-T7, with vertebral osteomyelitis and spondylitis. Microbiological assays identified E. cecorum cultured from spondylitic lesions. Affected flocks were treated with amoxycillin at 25 mg/kg in the drinking water for 5 days, resulting in decreased numbers of lame birds and culls. Ref

  • Case 3: Enterococcal Spondylitis in a Broilers On late September 2015, a number of 10 weeks old roosters with characteristic clinical signs of lameness and hock-sitting posture were autopsied. During thorough general routine post-mortem examinations, abnormalities like nodular masses correlated well with the hock-sitting posture and posterior paresis/paralysis were observed in joint spaces on the caudal thoracic vertebral column (T6-T7) immediately anterior to the kidneys in all affected birds. At histopathological examinations, osteomyelitis with limited pathological lesions including mononuclear inflammatory cells infiltration and edema in spinal cord were seen and the infection was diagnosed as an acute spondylosis. Ref

  • Case 4: Enterococcal Spondylitis in a Chickens Enterococcus cecorum was isolated from spondylitis lesions in broilers from two flocks in North Carolina that were experiencing increased mortality. Affected birds showed paresis and paralysis, clinical signs characteristic of enterococcal spondylitis (ES). Affected birds rested on their hocks and caudal abdomens with legs extended forward and were unable to stand or walk. Necropsy examination of affected birds revealed firm to hard inflammatory masses involving the vertebral bodies at the level of the free thoracic vertebra that bulged dorsally and compressed the spinal cord. When opened, lesions contained pale, tan to yellow caseonecrotic material. Microscopically, necrosis and fibrinoheterophilic spondylitis with intralesional gram-positive bacteria were seen. Heavy growth of E. cecorum recovered from vertebral lesions confirmed the diagnosis of ES. To investigate possible sources of the organism for one of the flocks bacterial cultures were made from the environment, water lines, mice trapped on the farm, cecal/cloacal swabs from one of the parent broiler breeder flocks, egg residue, hatching eggs, and the hatchery environment. Except for cecal/cloacal swabs from the breeders, E. cecorum was not isolated from any of these samples. When compared phenotypically and genotypically, cecal/cloacal isolates of E. cecorum from the breeders differed from isolates from spondylitis lesions in the broilers. The source of E. cecorum for the broiler flocks was not determined, but vertical transmission appears unlikely. Ref

  • Case 5: Enterococcal Spondylitis in a Chickens An outbreak of enterococcal-associated vertebral osteoarthritis (EVOA) in male broiler breeders occurred in several flocks in South Africa. Male birds aged 4 and 9 weeks displayed the common presentation of lameness, paresis or complete paralysis. Autopsies of culled birds revealed masses on caudal thoracic vertebrae T5-T7, with vertebral osteomyelitis and spondylitis. Microbiological assays identified E. cecorum cultured from spondylitic lesions. Affected flocks were treated with amoxycillin at 25 mg/kg in the drinking water for 5 days, resulting in decreased numbers of lame birds and culls. Ref

  • Case 6: Enterococcal Spondylitis in a Chickens In a flock of 18200 broilers, a decrease in flock uniformity was detected from 14 days post hatch onwards with affected chickens showing lameness and an increase in flock mortality up to 7.22% at day 33 post hatch. In the first 3 weeks post hatch, pericarditis and hepatitis were found as the main pathological changes in 27.6% and 9.8% of the examined broilers respectively. Femoral head necrosis and vertebral osteomyelitis were detected in the last week of the growing period with 10.3% and 2.3% respectively. Heart, liver, spleen, yolk sac and vertebral column of 59 broilers with pathological changes were subjected to bacteriological analysis. Enterococcus cecorum was isolated from 23 birds (39%), the first broiler was already positive at day 3 post hatch in the yolk sac. Ref

  • Case 7: Enterococcal Spondylitis in a Chickens In September 2015, a number of 10 weeks old roosters with characteristic clinical signs of lameness and hock-sitting posture were autopsied. During thorough general routine post-mortem examinations, abnormalities like nodular masses correlated well with the hock-sitting posture and posterior paresis/paralysis were observed in joint spaces on the caudal thoracic vertebral column (T6-T7) immediately anterior to the kidneys in all affected birds. At histopathological examinations, osteomyelitis with limited pathological lesions including mononuclear inflammatory cells infiltration and edema in spinal cord were seen and the infection was diagnosed as an acute spondylosis. Ref

  • Case 8: Enterococcal vertebral osteomyelitis in a Chickens Diagnosed in 27-day-old broiler chickens submitted for lameness and depression. The broilers were crouched and sitting on their hocks. Enlarged thoracic vertebrae and intervertebral junctions were noted at necropsy. Spondylitis and osteomyelitis was confirmed microscopically. Enterococcus cecorum was isolated from vertebral cultures. Small bursas were also observed and an endemic strain of infectious bursal disease virus was detected by RT-PCR. Ref

  • Case 9: Enterococcal-related vertebral osteoarthritis in a Chickens Infections in broilers and broiler breeders by Enterococcus cecorum, causing clinical disease, have increasingly been described in various countries in the Northern Hemisphere over the past decade. This case report describes an outbreak of enterococcal-associated vertebral osteoarthritis (EVOA) in male broiler breeders in several flocks in South Africa. Male birds aged 4 and 9 weeks displayed the common presentation of lameness, paresis or complete paralysis. Autopsies of culled birds revealed masses on caudal thoracic vertebrae T5-T7, with vertebral osteomyelitis and spondylitis. Microbiological assays identified E. cecorum cultured from spondylitic lesions. Affected flocks were treated with amoxycillin at 25 mg/kg in the drinking water for 5 days, resulting in decreased numbers of lame birds and culls. The origin and pathogenesis of EVOA are poorly understood, which limits prevention to environmental factors that may inhibit systemic access by the enteric bacteria. Skeletal growth trends of male birds are thought to increase their susceptibility to bacterial colonisation at sites of skeletal strain, resulting in abscesses and lesions. Evidence points to the emergence of E. cecorum strains with increased pathogenicity; this highlights the need for greater understanding of the origins, treatment and prevention of EVOA to minimise its economic impact on poultry Ref

Treatment

NameSummary
Supportive careIsolate the bird from the flock and place in a safe, comfortable, warm location (your own chicken "intensive care unit") with easy access to water and food. Limit stress. Call your veterinarian.
AntibioticsBased on antimicrobial susceptibility testing

Support

Prevention

  • Reduce stress
  • Probiotics

Prognosis

Poor

Scientific References

Age Range

It occurs in 5-8 week old 'broiler' breeds

Risk Factors

  • Rapid growth: The growth plates of fast-growing species of poultry (meat-type chickens, turkeys) are extremely susceptible to bone damage.
  • Trauma
  • Immunosuppression caused by infectious and non-infectious factors
  • History of non-infectious bone condition
  • Unbalanced diet
  • Raising chickens on wire flooring
  • Male chickens have a higher risk.