AFIP SYSTEMIC PATHOLOGY

JPC SYSTEMIC PATHOLOGY

NERVOUS SYSTEM

April 2014

N-T08

 

Signalment (JPC #1372658) Slide A:  Pig; age, breed and gender unspecified

 

HISTORY:  This is one of a group of pigs whose water had been turned off for 3 consecutive days; when the farmer noticed that the water had been turned off, he immediately turned it back on; later that day the farmer noticed that many of the pigs were depressed, down or dead.

 

HISTOPATHOLOGIC DESCRIPTION:  Cerebrum:  Multifocally, there is multifocal laminar cortical necrosis characterized by disruption, loss and cavitation of the middle to deep cortical gray matter, loss of neurons and replacement by eosinophilic and karyorrhectic debris.  Within areas of necrosis, there are many gitter cells, increased numbers of microglia, fewer reactive astrocytes and a few scattered gemistocytes (gliosis).  Within less affected areas, many neurons are hypereosinophilic, angular and shrunken with pyknotic nuclei (necrosis) and are frequently surrounded by a few glial cells (satellitosis).  Blood vessels within the neuropil are often prominent, lined by hypertrophic endothelium (reactive), and surrounded by variably dense cuffs of eosinophils, lymphocytes and macrophages.  Low numbers of similar inflammatory cells multifocally expand the leptomeninges. There is mild spongiosis within the subadjacent white matter. 

 

MORPHOLOGIC DIAGNOSIS:  Cerebrum, gray matter:  Laminar cortical necrosis, multifocal, with lymphoplasmacytic and eosinophilic perivascular encephalitis and gliosis, breed not specified, porcine

 

Signalment (JPC #1619720) Slide B:  Sheep; age, breed and gender unspecified

 

HISTORY:  This sheep was given a large quantity of water after having no access to water for 48 hours. 

 

HISTOPATHOLOGIC DESCRIPTION:  Cerebrum:  There is multifocal, laminar cortical necrosis of the middle to deep gray matter, characterized by vacuolation and loss of neuropil, neuronal necrosis and loss, with increased number of hypertrophic microglial cells and astrocytes (gliosis).  Within areas of necrosis, many neurons are hypereosinophilic, angular and shrunken with pyknotic nuclei (necrosis) and are occasionally surrounded by a few glial cells (satellitosis).  Virchow-Robin space is multifocally expanded by clear space and vessel endothelial cells are hypertrophic with swollen nuclei.

 

Cerebellum and brain stem:  No significant findings.

 

MORPHOLOGIC DIAGNOSIS B:  Cerebrum, gray matter:  Laminar cortical necrosis, multifocal, with multifocal spongiosis, breed not specified, ovine

 

ETIOLOGIC DIAGNOSIS:  Hypernatremic polioencephalomalacia

 

CAUSE:  Salt toxicity and water deprivation

 

GENERAL DISCUSSION:

·       Occurs primarily in pigs and poultry, and occasionally in ruminants

·       Sources of intoxication include ingestion of brackish or tidal water, oil well sludge and improperly mixed milk replacers

·       In cattle, chronic ingestion of water with moderate increases in salt content can result in infertility, reproductive losses and decreased milk production

·       In cold climates, can occur from freezing of water source

 

PATHOGENESIS:

Indirect salt poisoning: Consumption of high levels of salt, followed by water deprivation and then excessive water consumption

·       Occurs in swine

·       In sheep and cattle, based on circumstantial evidence only

·       Decreased water intake → dehydration and increased plasma sodium, which moves passively into CSF → high sodium inhibits anaerobic glycolysis in the brain → cerebral energy production decreased → sodium cannot be actively transported from CSF back to plasma → increased cerebral sodium creates osmotic gradient à edema, increased pressure, and necrosis result after regaining access to ion free water

·       Increased sodium causes cerebral eosinophilia in pigs(unknown mechanism)

·       Increased susceptibility of swine may be partly due to high level of dietary salt

Direct Salt Poisoning: Excessive consumption of water with high salt content, or excessive salt consumption after salt restriction

·       Occurs primarily in ruminants (primarily cattle) and poultry

·       Nervous signs, and gastrointestinal lesions due to osmotic disturbance, electrolyte influx and direct irritation

 

TYPICAL CLINICAL FINDINGS:

·       Swine:  Tremors, seizures, dog-sitting stance, blindness, deafness, unresponsive to external stimuli and head-pressing

·       Ruminants:  Vomiting, diarrhea, abdominal pain, polyuria, paresis, knuckling of fetlocks, and blindness; death may occur within 24 hours

 

TYPICAL GROSS FINDINGS:

·       Meningeal and cerebral edema and congestion; flattened cortical gyri

·       Gastric hyperemia, erosions and ulcerations

·       Severe congestion of mucosa of abomasum in cattle from direct salt poisoning

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

·       Swine

·       Cerebral edema

·       Laminar necrosis primarily in dorsolateral cortex

·       Eosinophils - leptomeninges, perivascular spaces

·       Prominent cerebral blood vessels lined by hypertrophied endothelium

 

·       Ruminants

·       Cerebral laminar cortical necrosis; cerebral edema; perivascular cuffing with mononuclear cells

·       In some cases, Purkinje cell necrosis; cerebral arteriolar degeneration with transmural neutrophils

·       Salt toxicity in ruminants does not consistently produce the characteristic cerebral eosinophilia seen in swine

 

·       Turkey

·       Multifocal and symmetric malacia and vacuolation of brain and spinal cord

 

ADDITIONAL DIAGNOSTIC TESTS:

·       Serum, cerebral, CSF and ocular sodium levels

 

DIFFERENTIAL DIAGNOSIS:

·       In swine, the combination of laminar cortical necrosis and eosinophilic meningeal and perivascular inflammation is pathognomonic for water deprivation/salt toxicity

·       Thiamine deficiency (thiaminase toxicity) results in similar lesions in ruminants

 

Other causes of encephalitis in swine include:

·       Pseudorabies/Aujeszky's disease (Herpesvirus suis):  Nonsuppurative meningoencephalomyelitis with ganglioneuritis, neuronal degeneration and necrosis, and intranuclear inclusion bodies; also multifocal necrosis in the liver, spleen and adrenal gland

·       Bacterial meningoencephalitis (Streptococcus suis, Haemophilus parasuis)

·       Teschen's disease (Porcine enterovirus):  Nonsuppurative polioencephalomyelitis

·       Arsenic toxicity:  Cerebral edema and hemorrhage from vascular necrosis, but primarily degeneration of the spinal cord, peripheral and optic nerves; hemorrhagic gastroenteritis

·       Porcine hemagglutinating encephalomyelitis virus (coronavirus): Nonsuppurative meningoencephalomyelitis and neuronal degeneration primarily within peripheral ganglia and the gray matter of the caudal brain stem and spinal cord

·       Rabies (rhabdovirus):  Nonsuppurative encephalomyelitis with perivascular lymphocytic cuffing, gliosis and Negri bodies

·       Edema disease (E. coli):  Shiga-like toxin damages endothelium, resulting in fibrinoid necrosis and vasculitis with secondary ischemic damage

 

COMPARATIVE PATHOLOGY:

·       Poultry: Can occur in waterfowl and other wild birds

·       Clinical signs include excessive thirst, respiratory distress and paralysis

·       Usually results in cerebral congestion and edema; occasionally necrosis

·       Also causes cystic testes, acute tubular necrosis, pulmonary hypertension syndrome and glomerulosclerosis

·       Dog and cat

·       Not associated with cerebral cortical necrosis

 

References:

1.      Cantile C, Youssef S. Nervous system.  In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. Philadelphia, PA: Elsevier; 2016:314-315.

2.      Carson TL. Toxic minerals, chemicals, plants, and gases. In: Straw BE, Zimmerman JJ, D’Allaire S, Taylor DJ, eds. Diseases of Swine. 9th ed. Ames, IA: Blackwell Publishing; 2006:980.

3.      Crespo R, Subbiah M, Corsiglia C, Bickford A, Puschner B. Avian diseases 2008; 52(179-182.

4.      Haschek WM, Rousseaux CG, Wallig MA. Fundamentals of Toxicologic Pathology. 2nd ed. London, UK: Academic Press; 2010:402.

5.      Miller AD, Zachary JF. Nervous system. In: Zachary JF, eds. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Mosby-Elsevier; 2017:853-854.

6.      Niles G. Sodium. In: Plumlee KH ed. Clinical Veterinary Toxicology. 1st ed. St. Louis, MO: Mosby; 2004: 218-221.

7.      Smith MO, George LW. Diseases of the nervous system. In: Smith BP, ed. Large Animal Internal Medicine. 4th ed. St. Louis, MO: Mosby Elsevier; 2009:1026.

8.      Summers BA, Cummings JF, de Lahunta A. Veterinary Neuropathology. St. Louis, MO: Mosby; 1995:254-255.

9.      Thompson LJ. Sodium chloride (salt). In: Gupta RC, ed. Veterinary Toxicology Basic and Clinical Principles. 1st ed. New York, NY: Academic Press; 2007:461-464.

 

 


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