NAVLE Nervous

Bovine Listeriosis Study Guide

Listeriosis (also known as Circling Disease or Silage Sickness) is a sporadic but serious bacterial infection caused by Listeria monocytogenes, a gram-positive, facultatively anaerobic, intracellular coccobacillus.

Overview and Clinical Importance

Listeriosis (also known as Circling Disease or Silage Sickness) is a sporadic but serious bacterial infection caused by Listeria monocytogenes, a gram-positive, facultatively anaerobic, intracellular coccobacillus. The disease primarily manifests as encephalitis or meningoencephalitis in adult cattle, though it can also cause abortion and septicemia. This condition is particularly important for the NAVLE because it requires differentiation from other neurological diseases including rabies, polioencephalomalacia, and thromboembolic meningoencephalitis.

Listeriosis is a zoonotic disease with significant public health implications. Veterinarians treating affected cattle must take appropriate precautions, as humans can become infected through contaminated milk or direct contact with infected animals and tissues. The disease is most commonly associated with feeding poorly preserved silage with a pH greater than 4.0 to 5.5.

Risk Factor Clinical Significance
Poorly fermented silage (pH greater than 4.0-5.5) Primary risk factor; Listeria thrives at higher pH where lactic acid fermentation is inadequate
Soil contamination of feed Silage harvester picks up soil; more prevalent after wet summers with difficult harvesting conditions
Aerobic deterioration of silage Oxygen exposure at silage surface or from poor sealing promotes Listeria growth
Bale silage versus pit silage Higher risk with bale silage due to typically higher pH and more variable fermentation
Oral mucosal damage Tooth eruption, dosing gun injuries, or feeding coarse feeds creates entry points for bacteria
Immunosuppression and stress Poor nutrition, transportation stress, pregnancy, and parturition increase susceptibility

Etiology

Causative Organism

Listeria monocytogenes is the primary causative agent. Key characteristics include:

  • Gram-positive, non-spore-forming, motile coccobacillus
  • Facultatively anaerobic and facultatively intracellular pathogen
  • Catalase-positive and oxidase-negative with beta-hemolysis on blood agar
  • Capable of growth at refrigeration temperatures (4°C to 44°C), which is diagnostically significant (cold enrichment technique)
  • Characteristic tumbling motility when viewed microscopically at room temperature (20-25°C)
  • Ubiquitous in the environment: soil, water, decaying vegetation, silage, and GI tracts of healthy animals
High-YieldL. monocytogenes survives intracellularly within macrophages by using listeriolysin O to escape from phagosomes. This intracellular location makes antibiotic treatment challenging and explains why high doses and prolonged treatment are necessary.
Form Population Affected Key Features
Encephalitic (most common) Adult cattle, often 1-3 years old Unilateral cranial nerve deficits, circling, depression; course 1-2 weeks
Abortion Pregnant cows, usually last trimester Sporadic abortions, retained placenta; autolyzed fetus with hepatic necrosis
Septicemia Neonatal calves (less than 3 weeks) Acute illness, fever, hepatic necrosis, hemorrhagic gastroenteritis; often fatal
Keratoconjunctivitis (Silage Eye) Any age cattle exposed to dusty silage Conjunctivitis, keratitis, uveitis from direct contamination

Epidemiology

Distribution and Occurrence

  • Geographic distribution: Worldwide, but more common in temperate and colder climates
  • Seasonality: Winter-spring disease (December to May in Northern Hemisphere), coinciding with silage feeding season
  • Age predisposition: More common in younger animals (1-3 years old), associated with tooth eruption and emergence of permanent molars
  • Herd impact: Usually sporadic (1-2 animals affected), but outbreaks can affect up to 10-20% of herd
  • Carrier state: High incidence of asymptomatic intestinal carriers that shed bacteria in feces

Risk Factors

Cranial Nerve Function Affected Clinical Signs
CN V (Trigeminal) Facial sensation, mastication Dropped jaw (motor), decreased facial sensation, food impaction in mouth
CN VII (Facial) Facial muscle movement Drooping ear, flaccid lip, deviated muzzle, lowered eyelid, absent menace response, drooling
CN VIII (Vestibulocochlear) Balance, coordination Head tilt toward affected side, circling toward affected side, nystagmus, ataxia
CN IX/X (Glossopharyngeal/Vagus) Swallowing, pharyngeal function Dysphagia (difficulty swallowing) - dramatically worsens prognosis
CN XII (Hypoglossal) Tongue movement Tongue protrusion, paralysis

Pathogenesis

Route of Infection and Neural Invasion

The pathogenesis of encephalitic listeriosis is unique and involves ascending infection via the trigeminal nerve. This distinctive mechanism explains the characteristic unilateral clinical signs and brainstem localization.

  • Ingestion: Cattle ingest contaminated silage or pasture material containing L. monocytogenes
  • Mucosal entry: Bacteria enter through breaks in oral mucosa (tooth eruption sites, wounds, abrasions)
  • Axonal invasion: L. monocytogenes invades sensory nerve endings of the trigeminal nerve (CN V)
  • Centripetal migration: Bacteria travel within axons (intra-axonal transport) to the trigeminal nucleus in the pons
  • Brainstem infection: Bacteria multiply in the pons and medulla oblongata, causing microabscessation and inflammation
  • Cranial nerve involvement: Inflammation damages cranial nerve nuclei (CN V, VII, VIII primarily), producing characteristic unilateral deficits
NAVLE TipThe unilateral nature of clinical signs is a KEY diagnostic feature of listeriosis. Unlike most CNS diseases that produce bilateral or symmetric signs, listeriosis typically affects one side more severely because bacteria ascend through ONE trigeminal nerve. Look for asymmetric facial paralysis, head tilt, and circling toward the affected side.
CSF Parameter Expected Finding Notes
Total nucleated cell count Mild to moderate increase Highest TNCC among cattle CNS diseases
Cell type Predominantly mononuclear (despite bacterial cause) May see mixed pleocytosis; lymphocytes predominate
Protein concentration Moderately elevated Highest protein among cattle CNS diseases
Glucose Slightly decreased Bacterial consumption of glucose
Culture/PCR Often negative Listeria rarely reaches meningoventricular system; isolation difficult

Clinical Presentation

Forms of Listeriosis in Cattle

Clinical Signs of Encephalitic Listeriosis

Early Signs

  • Depression and dullness (ascending reticular activating system involvement)
  • Anorexia and decreased water intake
  • Fever (variable; often present early but may be absent in advanced cases)
  • Isolation from herd

Classic Unilateral Neurological Signs

Additional Neurological Signs

  • Circling: Compulsive movement toward the affected side (hence "Circling Disease")
  • Head pressing: Animal pushes head against fixed objects, walls, or corners
  • Profuse salivation: Continuous drooling due to inability to swallow and facial paralysis
  • Ipsilateral weakness: Paresis on the same side as other deficits (long tract involvement)
  • Behavioral changes: Occasional excitement or aggression, disorientation

Terminal Signs

  • Recumbency (animal unable to stand)
  • Convulsions and opisthotonus
  • Coma and death
Differential Distinguishing Features Key Difference
Rabies Behavioral changes, aggression, progressive paralysis, exposure history ALWAYS consider; may look identical; no unilateral pattern
Polioencephalomalacia (PEM) Cortical blindness, dorsomedial strabismus, seizures, responds to thiamine Bilateral signs; no cranial nerve deficits
Thromboembolic Meningoencephalitis (TEME) Histophilus somni infection; feedlot cattle; retinal hemorrhages; rapid death Vasculitis present; no facial paralysis
Lead Poisoning Blindness, head pressing, jaw champing, lead exposure history Bilateral signs; no facial paralysis
Pregnancy Toxemia/Ketosis Late pregnancy or early lactation; ketotic odor; elevated BHB No facial or ear paralysis; BHB greater than 3 mmol/L
Brain Abscess/Coenurosis Circling, blindness (contralateral), proprioceptive deficits No cranial nerve deficits

Diagnosis

Clinical Diagnosis

Presumptive diagnosis is based on the classic triad of: history of silage feeding + unilateral cranial nerve deficits + depression. This is often sufficient to initiate treatment while awaiting confirmatory testing.

Cerebrospinal Fluid (CSF) Analysis

CSF analysis from lumbosacral collection supports the diagnosis but is not definitive:

Definitive Diagnosis

Definitive diagnosis requires postmortem examination:

  • Gross pathology: Often minimal findings; may see mild meningeal congestion or softening (malacia) of brainstem
  • Histopathology (gold standard): Microabscesses (foci of neutrophils and macrophages), perivascular cuffing (mononuclear cells), and gliosis localized to pons and medulla oblongata
  • Gram stain: May reveal gram-positive coccobacilli, but often few organisms visible
  • Immunohistochemistry (IHC): Superior to culture (84% positive by IHC vs 39% by culture); detects listeriolysin O antigen
  • Bacterial culture: From brainstem tissue; may use cold enrichment technique (incubation at 4°C)
  • PCR: Molecular detection from brain tissue increasingly used

Exam Focus: Histopathologic lesions in listeriosis are ASYMMETRIC and LOCALIZED to the BRAINSTEM (pons and medulla). Key features are: microabscesses, perivascular mononuclear cuffing, and malacia. The unilateral nature of lesions correlates with the unilateral clinical signs. Immunohistochemistry is superior to culture for confirmation.

Drug Dosage Notes
Procaine Penicillin G (first-line) Intensive phase: 40,000-80,000 IU/kg IV q6-8h for 3-5 days Maintenance phase: 22,000 IU/kg IM q12h for 14-21 days Drug of choice; high doses required to achieve bactericidal CNS concentrations
Oxytetracycline (alternative) 10-20 mg/kg IV q12-24h Alternative if penicillin not available; bacteriostatic
Ampicillin 10-20 mg/kg IV q6-8h Used in combination with aminoglycosides in human medicine

Differential Diagnosis

NAVLE TipThe KEY differentiating feature of listeriosis is UNILATERAL cranial nerve deficits (especially facial and ear paralysis). PEM, lead poisoning, and pregnancy toxemia all produce BILATERAL signs. RABIES must ALWAYS be on the differential list for any bovine neurological case - handle with appropriate precautions and submit brain for testing if rabies cannot be ruled out.
Factor Better Prognosis Worse Prognosis
Ambulatory status Standing; 77% survival if ambulatory Recumbent; only 2/9 recumbent animals survive
Swallowing ability Intact swallowing reflex Dysphagia present; dramatically worsens outcome
Treatment timing Early treatment within first 24-48 hours Delayed treatment; advanced CNS damage
Species Cattle: ~50-70% survival with treatment Small ruminants: 26-30% survival
Menace response Present menace response Absent or weak menace response

Treatment

Antimicrobial Therapy

Treatment success depends on early intervention before extensive brainstem damage occurs. The intracellular nature of L. monocytogenes and blood-brain barrier penetration requirements necessitate high doses and prolonged treatment (2-4 weeks).

Supportive Care

  • Fluid therapy: Correct dehydration and electrolyte imbalances from anorexia and excessive salivation
  • Acid-base correction: Sodium bicarbonate IV if metabolic acidosis present (loss of saliva buffer)
  • Thiamine (Vitamin B1): 5-10 mg/kg to support nervous tissue and rule out concurrent PEM
  • NSAIDs: Flunixin meglumine (2.2 mg/kg IV) for anti-inflammatory effects
  • Nutritional support: Rumen transfaunation; stomach tube feeding if dysphagia not severe
  • Eye care: Lubrication for exposure keratitis if eyelid paralysis present
  • Nursing care: Prevent secondary musculoskeletal injury; deep bedding for recumbent animals

Prognosis

High-YieldRECUMBENCY and DYSPHAGIA are the two strongest negative prognostic indicators. If an animal is still standing and can swallow, aggressive early treatment has a reasonable chance of success (up to 70-77% survival in cattle). Once recumbent, survival drops dramatically to approximately 10-20%.

Prevention and Control

Silage Quality Management

The cornerstone of listeriosis prevention is proper silage management to achieve adequate fermentation and prevent Listeria proliferation:

  • Target silage pH less than 4.5: Listeria cannot survive at low pH; proper lactic acid fermentation is critical
  • Minimize soil contamination: Raise cutting height, avoid muddy fields, maintain equipment
  • Ensure adequate packing density: Proper compaction reduces oxygen and promotes anaerobic fermentation
  • Proper sealing: Use quality plastic covers; prevent air ingress during storage
  • Appropriate moisture content: Not too wet (favors clostridial growth) or too dry (poor fermentation)
  • Use silage additives: Formic acid or bacterial inoculants (lactic acid bacteria) improve fermentation
  • Discard spoiled silage: Do not feed moldy, aerobically deteriorated, or visibly spoiled material

Additional Prevention Measures

  • Remove affected silage from ration if cases occur (may prevent additional cases)
  • Feed from troughs rather than directly on ground (pasture-associated cases)
  • Avoid feeding silage to young animals during tooth eruption period if possible
  • No effective vaccine is commercially available for cattle
  • Good hygiene practices; proper disposal of aborted material

Zoonotic Considerations

Listeriosis is a significant zoonotic disease. Veterinarians and farm workers are at risk when handling affected animals or contaminated materials:

  • Human infection routes: Contaminated milk, soft cheeses, ready-to-eat foods; direct contact with infected tissues
  • High-risk groups: Pregnant women (risk of abortion, neonatal infection), elderly, immunocompromised individuals
  • Protective measures: PPE when handling affected animals; proper hygiene; avoid raw milk consumption
  • Milk withholding: Extended withdrawal times due to high-dose antibiotic treatment; consult FARAD

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