|Disease||Agent||Clinical signs||Diagnostic aids
(genotypes) of (usually hemolytic)
|Onset often within 2 weeks of weaning. Ataxia, incoordination, mental confusion, recumbency, perhaps edema of eyelids, face, nose or lips. Most die within two days. Chronic: Head tilt, incoordination, unthriftiness.||Edema, if present, a useful lesion. At necropsy, edema in stomach wall and spiral colon in some. Culture gut for hemolytic E. coli and genotype isolate for shiga-like toxigenicity. Chronics may have encephalomalacia in brain stem.|
|Teschovirus infections||Teschovirus||Most outbreaks in Europe; Teschen Disease: High morbidity and mortality in all age groups. Ataxia leading to paralysis. Opisthotonus, convulsions, nystagmus, coma, death.
Talfan Disease: Similar but less severe and only in young pigs. In US,
posterior paralysis occasionally seen.
|Isolate and identify serotype. Histopath lesions and their distribution are suggestive of diagnosis. In the US, few highly pathogenic strains but most herds have endemic infections of low virulence.|
|Hemagglutinating encephalomyelitis||Coronavirus||Piglets < 4 weeks: Vomiting, retching, dehydration, wasting, coma, death.
Encephalitic form: Same, followed by tremors, hyperesthesia, dog-sitting, walking backwards, nystagmus, convulsions, recumbency, paddling with legs, bloating, coma, death. Mortality can approach 100%.
|Isolate and identify virus from brain of early, acute case. Histopath of value. Serial blood samples may show rising titers to virus. Many herds in the US endemically affected but outbreaks are uncommon.|
|Phenylarsonic compound (organic arsenic) poisonings||Arsanilic acid and roxarsone||Acute: Convulsions following exercise; incoordination progressing to paraplegia. No blindness.
Chronic: Ataxia and incoordination leading to paralysis. Blindness if from arsanilic acid.
|Signs and history of overmedication or misuse often adequate for diagnosis.
Histology: Demyelinating lesions of cord and peripheral nerves are suggestive. Prompt analysis of kidney, liver, urine and ration may identify excessive levels.
|Herpesvirus||Neonates < 3 weeks: Incoordination, ataxia, salivation, opisthotonus, seizures, recumbency with paddling. Sudden death common.
Older pigs: Similar but less severe signs. Naïve growers/finishers/adults: respiratory signs or abortions. CNS signs may occur sporadically and vary in severity.
|Consider signs in all age groups and area history of disease. Virus isolation and identification from tonsil, brain, spleen, liver, lung, cervical nodes. A reportable disease with national/state/industry
|Streptococcal meningitis||Streptococcus suis||Weaners/growers: Incoordination, tremors, opisthotonus, convulsions, blindness,
|Culture brain and cerebrospinal fluid. Identify the organism. Histopath of brain is helpful. Polyarthritis, myocarditis and pneumonia often present. May be endemic in herd.|
(Too much salt; or water deprivation)
|Acute onset, many affected. Aimless wandering, blindness, deafness, dog-sitting, convulsions, prostration with paddling, coma, death.||History of water restriction or deprivation followed by unrestricted access. Ration can have normal levels of salt.
Diagnosis: Histopathology and chemistry of the brain.
Key: * Other less frequent association of CNS signs include acute classical swine fever in young growing pigs, CNS metastases of pasteurellae, E. coli, Haemophilus parasuis, Salmonella serotypes, also viral infection including rabies, and toxicities (organophosphate, carbamate, chlorinated hydrocarbons). Male Landrace and Landrace-cross piglets and British Saddlebacks of either sex sometimes have a genetic defect that may result in CNS signs.