JPC SYSTEMIC PATHOLOGY
Signalment (D86-608): 12-day old chick
HISTORY: This chick had paralysis beginning at 10 days of age.
HISTOPATHOLOGIC DESCRIPTION: Slide A: Multiple sections of brain including optic lobe, cerebellum and multiple sections of cerebrum.
1. Cerebrum: Predominately within the superficial cortex and rarely in the deeper cortex, there are moderate numbers of necrotic neurons that are hypereosinophilic, shrunken and angular with pyknosis or karyolysis, and fewer degenerate neurons with central chromatolysis, admixed with many astrocytes and glial cells which often surround affected neurons (satellitosis). Multifocally and predominately within the gray matter are few glial nodules and gliosis (characterized by focal aggregates and overall increased numbers of glial cells, respectively). Multifocally Virchow-Robin spaces and the meninges are mildly expanded by few lymphocytes, macrophages and plasma cells which multifocally extend into the surrounding parenchyma. The choroid plexus is focally infiltrated by few heterophils.
2. Cerebellum: Many Purkinje cells are hypereosinophilic and shrunken with loss of nuclear detail (necrosis) and are often surrounded or replaced by few glial cells and rare lymphocytes and plasma cells. Within the molecular layer are few glial nodules. Multifocally within cerebellar gray and white matter, vessels are surrounded by few lymphocytes and plasma cells, which often infiltrate the adjacent parenchyma. Multifocally, the meninges are infiltrated by low numbers of lymphocytes, macrophages and plasma cells.
MORPHOLOGIC DIAGNOSIS: 1. Brain, cerebrum: Meningoencephalitis, lymphoplasmacytic, multifocal, mild, with neuronal degeneration and necrosis; gliosis; and mild heterophilic choroiditis, breed unspecified, chicken.
2. Brain, cerebellum: Purkinje cell necrosis, multifocal with gliosis and lymphoplasmacytic meningoencephalitis.
HISTOPATHOLOGIC DESCRIPTION: Slide B: Proventriculus (2 sections), ventriculus, intestine (2 sections), pancreas, mesentery, heart (2 sections):
1. Proventriculus: Multifocally, there are nodular aggregates of lymphocytes expanding the tunica muscularis and the lamina propria and compressing adjacent tissue.
2. Ventriculus: Multifocally separating myocytes are lymphoplasmacytic cellular infiltrates that separate myofibers in the muscular tunics. The inflammatory cells are oriented along fascial planes and frequently surround blood vessels.
3. Pancreas: Multifocally there are perivascular, nodular infiltrates of low to moderate numbers of lymphocytes.
4. Heart: Multifocally the myocardium is infiltrated by low to moderate numbers of lymphocytes, plasma cells, and fewer macrophages and heterophils. Few myocardial fibers are hypereosinophilic with loss of cross-striations and pyknosis (necrosis) or rarely, pale, swollen and vacuolated (degeneration). Pericardial adipose tissue contains similar inflammatory infiltrates.
5. Small intestine: Focally and markedly expanding the lamina propria of few blunted and fused villi are abundant lymphocytes, histiocytes, frequent mitotic figures and fewer heterophils which surround and separate tortuous, hyperplastic crypts. Crypt hyperplasia is characterized by increased numbers of mitotic figures and piling up of the epithelium. Multifocally, surrounding the affected crypts are many lymphocytes and histiocytes with frequent mitotic figures. Multifocally within the epithelium are few degenerate heterophils.
MORPHOLOGIC DIAGNOSIS: 1. Proventriculus and ventriculus: Proventriculitis and ventriculitis, lymphoplasmacytic, multifocal, mild, breed unspecified, chicken.
2. Heart: Myocarditis, lymphohistiocytic and heterophilic, multifocal, mild with multifocal necrosis and degeneration.
3. Pancreas: Pancreatitis, perivascular, lymphocytic, multifocal, mild.
4. Small intestine: Enteritis, lymphohistiocytic and heterophilic, focal, mild with crypt hyperplasia.
ETIOLOGIC DIAGNOSIS: Picornaviral encephalomyelitis
CAUSE: Avian encephalomyelitis virus (AE)
CONDITION: Infectious avian encephalomyelitis
CONDITION SYNONYMS: Epidemic tremor
· Avian encephalomyelitis (Picornaviridae, Tremorvirus) - Worldwide viral infection of young (usually 1-3 weeks old) chickens, turkeys, pheasants, and quail resulting in ataxia that can progress to paralysis and tremors of head and neck
· Adult infection results in decreased egg production and hatchability
· Morbidity may reach 60%; mortality rates are 25-50%
· Severity of disease depends on age and immunologic status of bird; birds younger than 3-5 weeks and immunocompromised animals are more severely affected
· Infected adult layers transmit the virus vertically with surviving chicks transmitting the virus horizontally in the feces
· Only young birds without maternal antibodies or those that are not immunocompetant develop life-long CNS signs
· Intestinal signs develop only in producing birds
· Horizontal infection results in replication in intestinal mucosa and lymphoid tissue resulting in viremia and dissemination to many other tissues (skeletal muscle, pancreas, other viscera) and finally the brain
· Transmission to adults is unknown, but believed to be through infected people or fomites; virus can survive long periods in environment
· After 6-weeks of age, birds are usually protected via increased immunocompetence and protective humoral response
TYPICAL CLINICAL FINDINGS:
· Decreased egg production and hatchability
· Survivors can develop cataracts around 18-20 weeks of age
· Ataxia and incoordination
· Fine tremors of the head and neck may develop (accentuated if startled)
TYPICAL GROSS FINDINGS:
· Often none
· Whitish areas in ventriculus muscle due to masses of infiltrating lymphocytes
· Survivors often develop a bluish lens opacity and have impaired vision
TYPICAL LIGHT MICROSCOPIC FINDINGS:
· Pathognomonic: Central chromatolysis of neurons in brainstem (medulla oblongata)
· Disseminated non-suppurative encephalomyelitis
· Ganglionitis of dorsal nerve root ganglia
· Perivascular infiltration of small lymphocytes in brain and spinal cord except the cerebellum where lesions are confined to the nucleus cerebralis
· Nodular and diffuse microgliosis predominately in cerebellar molecular layer
· Degeneration of Purkinje cells
· Dense nodules of lymphocytes within muscular wall of the proventriculus (pathognomonic), ventriculus and within myocardium (esp. atrium)
· Increased number and size of lymphoid follicles in pancreas
· Neuronal vacuolization of granular endoplasmic reticulum
· Loss of attached and free ribosomes
· Destruction of Golgi cisternae
· Vacuolization of mitochondria and loss of cristae
· Virus ~25 nm hexagonal; forms paracrystalline arrays
ADDITIONAL DIAGNOSTIC TESTS:
· History, age and typical clinical CNS signs suggest AE
· Indirect fluorescent antibody (IFA), virus isolation (VI), ELISA, virus neutralization
· Marek’s disease (herpesvirus): Ventricular muscular opacities (masses of infiltrating lymphocytes); lymphocytic infiltration in peripheral nerves very rarely seen in AE infection
· Marek’s disease (alphaherpesvirus, Herpesviridae): Lymphoid infiltrates in the peripheral nerves and lymphomatosis of viscera
· Newcastle disease (rubulavirus, Paramyxoviridae): Peripheral chromatolysis
· Avian influenza (Influenza virus type A, Orthomyxoviridae): Associated lesions of necrosis and inflammation of dermis with hydropic degeneration and bulla formation in the epidermis and wattles
· Equine encephalitis virus (alphavirus, Togaviridae): High morbidity/mortality
· West Nile Virus: Hemorrhage in cerebellar folia, cerebrum, brain stem, cervical spinal cord; Degeneration and necrosis of cerebellar molecular layer and Purkinje cells; lymphoplasmacytic meningoencephalitis; perivascular cuffing; gliosis
· Vitamin E deficiency: Swollen cerebellum with congestion, hemorrhage and necrosis
· Riboflavin deficiency: Myelin degeneration, Schwann cell proliferation
· Other avian species may be susceptible to natural infections
Genera of Picornaviridae:
o Foot and mouth disease
o Equine rhinitis A virus (formerly equine rhinovirus 1)
o Bovine rhinitis B virus
· Avihepatovirus: Duck hepatitis A virus
· Cardiovirus: Encephalomyocarditis swine/elephants; Theiler’s murine encephalomyelitis virus (Theilovirus)
o Pigs: Swine vesicular disease (SVD); Porcine enterovirus A & B
o Mice: Poliomyelitis (mouse encephalomyelitis, Theiler’s disease)
o Bovine: Bovine enterovirus infection
o Duck: Duck hepatitis virus
o Primates: Poliomyelitis
· Hepatovirus: Human & simian hepatitis A virus
· Teschovirus: Porcine teschovirus (formerly porcine enterovirus-1)
· Parechovirus or Erbovirus (undecided): Equine rhinitis B (formerly equine rhinovirus 2)
1. Calnek BW. Other viral infections: Avian encephalomyelitis. In: Saif YM, Fadly AM, Glisson JR, McDougald LR, Nolan LK, Swayne DE, eds. Diseases of Poultry. 12th ed. Ames, IA: Blackwell Publishing; 2008:430-441.
2. Charlton BR. Avian Disease Manual. 4th ed. New Bolton Center, PA: AAAP, University of Pennsylvania; 1996:14-16.
3. Gough RE, McNulty MA. Picornaviridae. In: Pattison M, McMullin PF, Bradbury JM, Alexander DJ eds. Poultry Diseases. 6th ed. Philadelphia, PA: Saunders Elsevier; 2008:350-354.
4. Ingram DR, Miller DL, et al. Serologic survey of wild turkeys (Meleagris gallopavo) and evidence of exposure to avian encephalomyelitis virus in Georgia and Florida, USA. J Wildl Dis. 2015; 51(2):374-379.
5. Senties-Cue CG, Gallardo RA, et al. Avian encephalomyelitis in layer pullets associated with vaccination. Avian Dis. 2016; 60(2):511-515.
6. Suarez DL. Avian encephalomyelitis. In: Swayne DE ed. Diseases of Poultry. 13th ed. Ames, IA: Wiley-Blackwell; 2013:486-493.
7. Summers BA, Cummings JF, de Lahunta A. Veterinary Neuropathology. St. Louis, MO: Mosby; 1995:123-125.
8. Swayne DE, Barnes JH, Abdul-Aziz T, Fletcher OJ. Nervous system. In: Avian Histopathology. 4th ed. Jacksonville, FL: AAAP; 2016:505-507.
9. Todd D, Weston JH, Mawhinney KA, Laird C. Characterization of the genome of avian encephalomyelitis virus with cloned cDNA fragments. Avian Dis. 1999; 43:219-226.