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Common Neurological Disorders of Food Animals

Food Animal Diseases and Management

Viral/Bacterial Causes
Rabies

  • Description: Fatal neurological disease affecting warm-blooded animals.

  • Reservoirs: Bats, dogs, foxes, skunks, and raccoons.

  • Transmission: Spread through bites (REPORTABLE).

  • Response: State officials will perform post-exposure response actions.

Clinical Signs:

  • Behavioral changes

  • Tenesmus (straining to defecate)

  • Salivation (possibly present)

  • Progressive lameness and ataxia

  • Posterior paresis (weakness or inability to move the hindquarters)

Forms of Rabies:

  • Furious Form: Characterized by aggressive behavior and extreme excitement.

  • Dumb Form: Characterized by lethargy and unresponsiveness.

  • Paralytic Form: Causes generalized paralysis.

Diagnosis:

  • Notify authorities upon suspicion.

  • Isolation of the affected animal.

  • Euthanasia may be necessary to prevent spread.

Tetanus

  • Causative Agent: Clostridium tetani.

  • Outbreaks are occasionally seen in young ruminants after:

    • Castration

    • Shearing

    • Docking

    • Vaccinations/injections

  • Other transmission methods include:

    • Surgical or traumatic wounds

    • Postpartum metritis (inflammation of the uterus).

Clinical Signs:

  • Change in gait (stiffness or abnormal movement)

  • Bloat (abnormal swelling)

  • Rigid extension of limbs

  • Raised tail head

  • Tetany of facial muscles (leading to dysphagia, retraction of lips and ears, trismus)

  • Locked jaw (trismus)

  • Prolapse of the third eyelid.

  • Symptoms worsen if the animal is startled or excited.

Diagnosis:

  • Presence of clinical signs such as muscular spasm and erect head posture.

  • History of wounds or recent surgery.

  • Direct smears from wound or spleen help confirm diagnosis: Look for large gram-positive rods with terminal spores.

Treatment:

  • Place the animal in a calm, dark environment.

  • Treatment principles include:

    • Elimination of bacteria

    • Neutralization of toxins

    • Relief of muscle spasms

    • Good nursing care

    • Establishment of active antitoxic immunity.

Prevention:

  • Prophylaxis not routinely prescribed for cattle due to low incidence.

  • In farms with multiple cases, tetanus toxoid inoculation may be recommended.

  • Vaccination is recommended in small ruminants.

Botulism

  • Causative Agent: Clostridium botulinum, resulting in flaccid paralysis.

  • Notable Occurrence: Often seen in herd outbreaks, particularly after feeding silage stored improperly (like in plastic bags).

  • Additional sources include:

    • Improper fermentation

    • Consumption of carrion or contaminated feed/products.

Clinical Signs:

  • Weak tongue tone

  • Dysphagia (difficulty swallowing)

  • Drooling

  • Generalized muscle weakness

  • Tremors

  • Recumbency (laying down)

  • Dilated pupils/poor pupillary light response.

Diagnosis:

  • Based on clinical signs and exclusion of other disorders.

  • Identification of spores in feed, feces, or GI contents.

  • Animals that die from this condition typically do not have pathological lesions.

Treatment:

  • Nutritional support for affected animals.

  • Nursing care for recumbent animals.

  • Bovine-origin antitoxin can be used (available on a limited basis).

Prevention:

  • A commercially available toxoid requires 3 doses administered 2-4 weeks apart.

  • Most herds do not get vaccinated routinely.

  • Ensure proper disposal of decaying silage and carcasses.

Listeriosis

  • Causative Agent: Listeria monocytogenes, a gram-positive rod.

  • Found in soil, silage, and feces; can cause microabscesses in the brain.

  • Outbreaks are more common in older animals, especially during the winter months.

Clinical Signs:

  • Depression

  • Fever and anorexia

  • Knuckling, weakness, or paralysis

  • Lip droop and inability to blink

  • Head tilt and nystagmus (uncontrolled eye movements)

  • Ataxia (lack of coordination) and dysphagia

  • Abortions, typically in late gestation.

Diagnosis:

  • Based on history and clinical signs (presumptive diagnosis).

  • Cytological analysis of cerebrospinal fluid (CSF) is the most useful test.

  • Definitive diagnosis often requires necropsy.

Treatment:

  • Antibiotics (penicillin, ampicillin, amoxicillin, aminoglycosides, macrolides)

  • NSAIDs for pain relief.

  • Supportive care including fluids and nutritional support.

Prevention:

  • Adequate silage preparation is crucial.

Diseases Caused By Deficiencies
Polioencephalomalacia

  • Caused by thiamine (Vitamin B1) deficiency.

  • Calves (2-12 months old) are at greatest risk.

  • Normal rumen microbial activity produces adequate thiamine under optimal conditions.

Risk Factors:

  • Grain overload or sudden dietary changes can lead to decreased thiamine production or increased destruction.

Mechanism:

  • Thiamine is essential for carbohydrate metabolism to glucose.

  • Deficiency leads to decreased glucose metabolism in the brain, causing cerebral edema and necrosis.

Clinical Signs:

  • Depression

  • Anorexia

  • Ataxia

  • Head-pressing

  • Dorso-medial strabismus (star gazing)

  • Recumbency, opisthotonus (abnormal posture), and convulsions.

  • High mortality within a few days if untreated.

Diagnosis:

  • Based on clinical signs and response to treatment (presumptive diagnosis).

  • Definitive diagnosis typically occurs during postmortem examination.

Treatment:

  • Thiamine supplementation, showing response within 2-12 hours.

  • Corticosteroids and mannitol to reduce cerebral edema.

  • Diazepam for convulsions.

Hypomagnesemia (Grass Tetany)

  • Caused by magnesium deficiency.

  • Can occur due to reduced food intake during adverse weather conditions, transport, or grazing low-Mg forage.

Clinical Signs:

  • Anorexia

  • Isolation

  • Hyperexcitability

  • Tetanic muscle spasms

  • Ataxia

  • Severe convulsions

  • Risk of death.

Diagnosis:

  • Based on clinical signs and history of exposure.

  • Response to therapy assists in verifying diagnosis.

Treatment:

  • IV administration of calcium borogluconate and magnesium hypophosphate.

  • Do not stimulate animal to rise for 30 minutes post-treatment.

  • Animals that recover typically do so within one hour of treatment.

Hypocalcemia (Milk Fever)

  • One of the most frequent metabolic diseases in dairy cattle.

  • Occurs mostly within 24 hours of calving.

  • Influenced by breed, age, and milk production levels.

Mechanism:

  • Sudden loss of calcium due to initiation of lactation.

Clinical Signs:

Stage I:

  • Mild excitement

  • Tetany without recumbency

  • Nervous behavior

  • Weak rumen contractions

  • Tachycardia

  • Hyperthermia

  • Shifting weight frequently.

Stage II:

  • Sternal recumbency with flaccid paralysis.

  • Depression

  • Fine muscle tremors

  • Cold extremities

  • Mild bloat and pupil dilation.

  • Loss of anal reflex and constipation.

Stage III:

  • Lateral recumbency with progressive loss of consciousness.

  • Severe bloating and compromised cardiac output.

Diagnosis:

  • Based on response to treatment and low serum calcium levels.

Treatment:

  • Stage I: oral calcium or IV calcium gluconate.

  • Stage II or III: immediate IV calcium gluconate administration.

Prevention:

  • Historically, lower calcium intake recommended during 10 days before calving.

Parasitic Causes
Cerebrospinal Nematodiasis in Ruminants

Cattle: Hypoderma bovis (Warble Flies)

  • Lifecycle: Larvae burrow through the skin, migrating to the spinal canal where they may remain dormant in epidural fat without causing neurological disease.

  • Risk: Dying larvae after treatment (organophosphate or avermectin dewormer) can release proteins causing edema and spinal cord inflammation.

  • Timing of Occurrence: Typically seen in North America between July and October.

Clinical Signs:

  • Symptoms often appear 24-72 hours post-anthelmintic administration.

  • Ataxia and weakness

  • Proprioceptive deficits

  • Altered reflexes (hind limbs most affected).

Diagnosis:

  • Based on clinical signs and history of parasitic treatment.

  • Definitive diagnosis only at necropsy with larva and lesions identification.

Treatment:

  • Symptomatic treatment: steroids and NSAIDs improve inflammatory responses.

  • Euthanasia may be necessary for severely damaged animals.

Prevention:

  • Proper timing of systemic anthelmintic grub treatments before larvae migrate to the epidural space.

Cerebrospinal Nematodiasis in Small Ruminants: Parelaphostrongylus tenuis

  • Endemic in Northeastern U.S. where white-tailed deer are common.

  • Migration into the CNS of deer is usually harmless, but aberrant migration in small ruminants results in severe spinal cord and brainstem disease.

Clinical Signs:

  • Paraplegia, paraparesis, tetraplegia, tetraparesis

  • Posterior ataxia progressing to recumbency

  • Brainstem disease: depressed sensorium, proprioceptive deficits, cranial nerve deficits.

Diagnosis:

  • Presumptive diagnosis through clinical signs and CSF evaluation.

  • Definitive diagnosis upon necropsy (parasites found in spinal cord).

Treatment:

  • Involves high doses of anthelmintics (ivermectin, fenbendazole, moxidectin).

  • Use of NSAIDs and dexamethasone to manage inflammatory responses.

  • Supportive care for nutrition and care for recumbent patients.

Prevention:

  • Regular deworming practices.

  • Reducing exposure to white-tailed deer.

Neosporosis

  • Causative Agent: Neospora caninum, causing neurological disease and abortions in ruminants.

  • Transmission: Dogs pass oocysts via feces; cattle ingest through contaminated food or water.

  • Lifelong infection in cattle, with tachyzoites that can infect the fetus through the placenta.

Clinical Signs:

  • Recumbency, lethargy, difficulty rising

  • Ataxia

  • Opisthotonus (abnormal postures)

  • Seizures

  • Affected calves are typically smaller than normal.

  • Clinical signs can appear mild at birth and progress over time.

Diagnosis:

  • Limited information on antemortem diagnosis.

  • Definitive diagnosis often made at necropsy.

  • Serological titers to assess the dam’s infection status.

Treatment:

  • No effective treatment available.

Prevention:

  • Prevent access of dogs to feed.

  • Cull seropositive cows.

Cerebellar Diseases

  • Categorized into three types:

    • In utero or neonatal viral infection.

    • Malformation of genetic or unknown causes.

    • Degenerative diseases (abiotrophies).

Clinical Signs:

  • Hypermetria (exaggerated limb movement)

  • Base-wide stance

  • Truncal ataxia (difficulty with posture control)

  • Intention tremor (tremors when reaching for an object).

Cerebellar Diseases - Viral Causes

  • Bovine Viral Diarrhea Virus: In calves, exposure can occur 90-170 days of gestation, resulting in inflammatory response and cellular destruction.

  • Border Disease Virus: Mainly affects sheep, transmitted through oronasal or transplacental routes. Clinical signs depend on the age of the animal at the time of infection.

  • Bluetongue Virus: Associated with severe CNS defects like hydranencephaly; cerebellar lesions may develop.

Genetic/Unknown Causes of Cerebellar Diseases

  • Caused by autosomal recessive traits found in various cattle breeds (e.g., Hereford, Shorthorn, Aberdeen Angus).

  • Premature death of cerebellar tissue occurs, with clinical signs appearing between 3-9 months of age (reported in Holstein, Charolais, Limousine, Angus breeds).

Nerve Injuries
Obturator Nerve Injury

  • Common complication of dystocia, particularly in first-calf heifers.

  • Caused by excessive force used during delivery of oversized, malpositioned fetuses.

  • Calving paralysis occurs when both obturator and sciatic nerves are damaged, resulting in a loss of adductor function and knuckling of distal hind limb joints.

  • Sensation is typically intact.

Clinical Signs:

  • Hopping gait and splay-legged posture

  • Cows unable to rise adopt a 'frog-like' sitting position.

  • Can lead to secondary injuries like femoral neck/shaft fractures and coxofemoral luxations.

Diagnosis:

  • Based on clinical history and signs presented by the animal (especially after calving).

Treatment:

  • Reduce inflammation using medications (e.g., dexamethasone, phenylbutazone).

  • Offer pain relief and ensure appropriate rest and footing for the animal.

  • Rotate recumbent animals several times a day to prevent further issues.

  • Hobbles may assist animals with minor deficits.

Diseases Caused by Prions
Bovine Spongiform Encephalopathy (BSE)

  • Commonly known as mad cow disease.

  • Affects both the brain of cattle and, potentially, humans.

  • Caused by abnormal proteins in brain tissue (prions) that induce fatal disease when ingested.

  • First identified in the UK in 1986, with outbreaks reported across Europe, Japan, Canada, and the USA.

  • Most cases (95%) occurred in the UK, primarily due to ingestion of contaminated ruminant meat and bone meal, banned in 1997 in the U.S.

Clinical Signs:

  • Hyperexcitability, anxiousness, heightened sensitivity to sound and touch.

  • Symptoms also include aggression, ataxia, and facial/ear twitching.

Diagnosis:

  • Based on historical context and observed clinical signs.

  • Confirmatory diagnosis requires histopathology of brain tissue (specifically at the obex).

Treatment:

  • Euthanasia is the recommended course of action.

Chronic Wasting Disease (CWD)

  • Affects deer, elk, reindeer, and moose across various ages.

  • Present in areas of North America, prions can persist in the environment for extended periods.

  • Progresses slowly, with clinical signs sometimes taking over a year to manifest.

  • Fatal with no treatments available.

Human Connection:

  • No strong evidence suggests CWD infects humans; however, the risk of transmission is not fully understood.

Transmission:

  • Via infected animal body fluids through direct contact or environmental contamination.

Clinical Signs:

  • Include wasting, lack of coordination, aggressive behavior, curiosity (fearlessness towards humans), excessive thirst/urination, drooling, listlessness, and drooped ears.

Diagnosis:

  • Clinical signs alone are not diagnostic but suggestive.

  • Definitive diagnosis requires examination of brain tissue at autopsy (obex).

Treatment:

  • No known treatment or vaccine available. CWD is also REPORTABLE.

Scrapie

  • A prion disease affecting sheep and goats primarily. Further details can be found in an associated article posted.