What causes encephalopathy in chickens?
Encephalopathy in chickens refers to diseases caused by damage to the brain tissue of chickens. The main manifestations are various neurological symptoms, such as head and neck tremors, ataxia, paralysis of the wings and legs, twisted neck, and circling. The causes are diverse, including bacterial, viral, metabolic, and toxic factors.
It is caused by Escherichia coli invading the brain tissue.
Necropsy shows soybean-sized grayish-white necrosis in the posterior part of the cerebral hemispheres, with depression.
Clinical symptoms include head and neck tremors, unstable standing, and so on.
For diagnosis, aseptically collect necrotic brain tissue, culture it on MacConkey medium, and red medium-sized colonies grow. Gram staining shows Gram-negative bacilli, and microscopic examination can usually confirm Escherichia coli.
For treatment, drug sensitivity testing is used to screen effective antibacterial drugs.
Also called cerebral pullorum disease, it is caused by Salmonella invading the brain tissue.
The necropsy changes and clinical symptoms are similar to those of Escherichia coli encephalitis. Microscopic examination can detect Gram-negative bacilli. When cultured on S.S. medium, small white colonies grow. Biochemical tests identify it as Salmonella pullorum.
Treatment is similar to that for Escherichia coli encephalitis.
Also called epidemic tremor. It is an infectious disease of the central nervous system caused by avian encephalomyelitis virus. It mainly affects chicks within 1 month of age.
Affected chicks show typical symptoms such as head and neck tremors, with a mortality rate of 10%-30%. Laying hens only show a transient drop in egg production, and chicks hatched from virus-carrying eggs show typical symptoms.
No characteristic lesions are visible to the naked eye in this disease, but histopathological changes have diagnostic significance, mainly central chromatolysis of nerve cells in the brainstem, especially the medulla oblongata, with changes of nonsuppurative encephalitis, formation of perivascular cuffs with cell infiltration, and proliferation of glial cells. In some internal organs, such as the myocardium, proventriculus, and gizzard, lymphoid follicle hyperplasia can be seen. A preliminary diagnosis can be made based on the age of onset and typical neurological symptoms such as head and neck tremors. Histopathological examination helps with diagnosis, and when necessary, virus isolation can be used for confirmation.
Vaccination of breeder flocks is an effective method to prevent this disease.
It is caused by Newcastle disease virus invading the brain tissue.
The main symptoms are twisted neck, paralyzed legs, opisthotonus, circling, and so on.
Necropsy shows congestion and hemorrhage of the meninges. Histopathological examination shows changes of nonsuppurative encephalitis. In addition, as features for differential diagnosis, chickens with Newcastle disease often show annular hemorrhage in the trachea, jujube-pit-like hemorrhage in the duodenum, and hemorrhage in the cecal tonsils and rectum.
The HI test can also be used to help with diagnosis.
3. Metabolic encephalopathy - encephalomalacia caused by Se-Ve deficiency
Se-Ve deficiency encephalopathy mainly affects chickens aged 2-4 weeks.
The main manifestations are ataxia, spasms of both legs, head tilted backward or nodding downward, or flapping wings while falling backward or rushing forward, and finally dying from spasms.
Necropsy shows edema and hemorrhage of the cerebrum, cerebellum, and medulla oblongata, swelling and softening of the brain parenchyma, appearing pale yellow, and in severe cases green. In addition to brain changes, necropsy commonly shows pancreatic necrosis, yellow gelatinous subcutaneous edema, and white striated necrosis of the pectoral muscles.
For treatment, Se-Ve powder can be mixed into the feed or "Dali Bu" can be given in drinking water, and the symptoms will disappear quickly.
Toxic encephalopathy is caused by toxic substances damaging the brain tissue. Substances that cause poisoning include moldy feed, chemical drugs, and so on. Moldy feed poisoning occurs because the feed contains large amounts of bacteria, molds, and the toxins they produce. Chemical drug poisoning may generally be caused by incorrect dosage calculation or uneven mixing.
After poisoning, the manifestations are excitement, rushing forward or backing up, and circling.
In addition to congestion and hemorrhage of the meninges, the necropsy changes are mainly hemorrhagic inflammation of the digestive tract, a distended gallbladder, incomplete blood coagulation, and more deaths among the heavier chickens in the flock.
If moldy feed and chemical drugs are stopped in time and large amounts of electrolytes and multiple vitamins are given, the condition will quickly improve.
In summary, when diagnosing such diseases, an in-depth and detailed investigation should be conducted into the epidemiology and feeding management of the flock, especially feed quality and nutritional composition, and the manifestations and characteristics of neurological symptoms should be observed. On the basis of clinical examination and necropsy, histopathological examination and pathogen isolation should be carried out. When poisoning is suspected, the possible factors and conditions of poisoning should be identified.