Severe myositis associated with avian encephalomyelitis in chickens
Andrew Brooks, Dominique Comeau, Jeff Caswell
Animal Health Laboratory, University of Guelph, Guelph, ON (Brooks), Department of Pathobiology (Comeau, Caswell)
AHL Newsletter 2021;25(4):17.
Two-week-old chickens with signs of neuromuscular disease were submitted to the Animal Health Laboratory (AHL) and the Department of Pathobiology, Ontario Veterinary College for postmortem examination. The clinical problems included reduced feed intake, runting, lethargy, and lameness. Approximately 10-15% of the flock was reluctant or unable to stand while others were alert and eating, but seemed less active than normal. The chickens were housed in a well-managed facility with regulated environmental temperatures and adequate access to feed and water. Hypoglycemia-spiking mortality syndrome or avian encephalomyelitis (AE) were suspected by the referring veterinarian.
The postmortem findings were nonspecific. Some birds were thin, and there was a wide variation in body weight. The crops were empty, and a small amount of feed and bedding material was present in the proventriculus and gizzard. The small and large intestines contained variable amounts of dark green liquid. Other findings included partially resorbed yolk sacs, mild splenic enlargement, and pulmonary congestion.
Histologically, there were prominent lesions in the skeletal muscle and heart. The muscle tissue was infiltrated with numerous lymphocytes and plasma cells. Myofibre necrosis and atrophy were especially severe in the skeletal muscle (Fig. 1). Skeletal muscle in the limbs, vertebral column, and esophagus was affected. In the gastrointestinal tract, there were infiltrates of lymphocytes and plasma cells in the muscular wall of the proventriculus, ventriculus, small intestine, and cecum. Such lesions in the proventriculus are considered pathognomonic for AE (Fig. 2). In contrast, the lesions in the nervous system were very mild. The brain contained occasional perivascular cuffs of lymphocytes and plasma cells, scattered foci of gliosis, and rare neuronal chromatolysis. Mild gliosis in the spinal cord and axonal degeneration in the peripheral nerves were also observed.
The diagnosis of AE was supported by the characteristic lesions in the viscera and CNS, and the detection of avian encephalomyelitis virus in the brain by PCR. Vaccination is an effective means of controlling AE, but the vaccination status of the source breeder flock for these chickens is not known. Hypoglycemia-spiking mortality syndrome was the other clinical differential diagnosis, but serum glucose concentrations were normal and compatible lesions were not observed.
Although myositis is known to occur with AE, the severity of myopathy in this case was unexpected, and it probably explains most of the clinical signs. The possibility of concurrent nutritional deficiency or ionophore toxicosis was considered, but the likelihood seemed low and further testing was not pursued. Skeletal muscle is not routinely sampled for histopathology when investigating AE. Over the past decade, 8 out of 18 AE cases in the AHL database included skeletal muscle in the histopathologic description; in all 8 cases there was inflammation, degeneration, and/or necrosis noted in the skeletal muscle, with varying degrees of severity. Although diagnostic lesions are typically found in the brain, spinal cord, and viscera, it is recommended to also include skeletal muscle for histopathology when investigating potential cases of AE in chickens. AHL
Figure 1. Skeletal muscle with lymphoplasmacytic inflammation, myofibre necrosis and atrophy. H&E.
Figure 2. Lymphoplasmacytic infiltration of the muscular wall of the proventriculus (arrow). This lesion is pathognomonic for avian encephalomyelitis. H&E.
Reference
Suarez DL. Avian encephalomyelitis. In: Diseases of Poultry, 14th ed. Swayne DE, ed. Wiley Blackwell, 2020;520-527.