NAVLE Nervous

Camelidae and Cervidae Listeriosis Study Guide

Listeriosis (also known as "circling disease" or "silage sickness") is a sporadic bacterial infection caused by Listeria monocytogenes, a gram-positive, facultative intracellular, non-spore-forming coccobacillus.

Overview and Clinical Importance

Listeriosis (also known as "circling disease" or "silage sickness") is a sporadic bacterial infection caused by Listeria monocytogenes, a gram-positive, facultative intracellular, non-spore-forming coccobacillus. While listeriosis is well-documented in traditional ruminants (sheep, goats, cattle), it occurs with

lower prevalence in camelids (llamas, alpacas) and cervids (deer species), but remains clinically significant due to its high mortality rate and zoonotic potential. The encephalitic form is the most commonly recognized presentation in these species, characterized by asymmetric brainstem lesions and cranial nerve deficits.

High-YieldListeriosis should be on your differential list for ANY camelid or cervid presenting with acute-onset asymmetric neurological signs, especially with history of silage feeding or during winter months. Remember: "Circling disease" = unilateral brainstem signs = think Listeria!
Factor Camelids Cervids
Prevalence Low compared to traditional ruminants; sporadic cases reported Uncommon; reported in white-tailed deer, moose, roe deer, fallow deer
Seasonality Winter-spring (associated with silage feeding) Winter-spring; may occur year-round in captive populations
Age Adults more common; neonatal septicemia in crias with FPT All ages; young animals may show septicemic form
Clinical Forms Encephalitis, septicemia (neonates), abortion, meningitis Encephalitis, septicemia, abortion (rare reports)

Etiology

Causative Agent

Listeria monocytogenes is the primary pathogen responsible for clinical listeriosis in camelids and cervids. Key characteristics of this organism include:

  • Gram-positive, facultatively anaerobic coccobacillus
  • Facultative intracellular pathogen (survives within macrophages)
  • Psychrophilic (can grow at refrigerator temperatures 4°C)
  • Motile via peritrichous flagella at 20-25°C but not at 37°C
  • Ubiquitous in environment (soil, water, decaying vegetation)
  • Produces listeriolysin O (LLO) - key virulence factor for intracellular survival

Epidemiology in Camelids and Cervids

System/Structure Clinical Signs Nerve(s) Affected
General Depression, anorexia, fever (early), obtundation Ascending reticular activating system
Facial Unilateral facial paralysis: drooping ear, drooping eyelid, flaccid lip, deviated muzzle CN VII (Facial)
Masticatory Dropped jaw, difficulty chewing, loss of facial sensation CN V (Trigeminal)
Vestibular Head tilt, nystagmus, circling toward affected side, ataxia CN VIII (Vestibulocochlear)
Pharyngeal Dysphagia, excessive salivation, regurgitation, tongue paralysis CN IX, X, XII
Ocular Absent menace response, strabismus, exposure keratitis (cannot blink) CN VI, VII

Pathogenesis

Route of Infection

The pathogenesis of encephalitic listeriosis involves a unique neural route that distinguishes it from most other bacterial CNS infections:

  • Ingestion: L. monocytogenes is ingested through contaminated feed (especially poorly fermented silage with pH greater than 5.0-5.5)
  • Mucosal Entry: Bacteria enter through small wounds or abrasions in the oral mucosa (often associated with dental eruption in young animals)
  • Neural Invasion: L. monocytogenes enters terminal branches of the trigeminal nerve (CN V) and migrates centripetally via retrograde intra-axonal transport
  • Brainstem Localization: Bacteria reach the trigeminal nucleus in the pons and medulla oblongata (rhombencephalon)
  • Local Spread: Infection spreads to adjacent cranial nerve nuclei (VII, VIII, IX, X, XII) causing characteristic unilateral deficits
NAVLE TipThe trigeminal nerve pathway explains why listeriosis causes UNILATERAL signs initially. Remember: Bacteria enter ONE side of the face, travel up ONE trigeminal nerve, and damage ONE side of the brainstem first. This asymmetry is your diagnostic clue!

Incubation Period

The incubation period is typically 10 days to 3 weeks following introduction of contaminated silage. The long incubation reflects the time required for retrograde axonal migration from the oral cavity to the brainstem. Outbreaks typically occur approximately 10 days after feeding poor-quality silage.

Form Clinical Features Species Affected
Septicemia Fever, depression, weakness, rapid death; neonates most susceptible Neonatal crias; young cervids
Abortion Late-term abortion; retained placenta; placentitis; minimal other signs Pregnant females (rare in camelids)
Keratoconjunctivitis "Silage eye": conjunctivitis, lacrimation, corneal opacity; may be self-limiting All species

Clinical Presentation

Encephalitic Form (Most Common)

The encephalitic form (rhombencephalitis) is the most frequently recognized presentation in both camelids and cervids. Clinical signs reflect asymmetric brainstem dysfunction and typically include:

Species-Specific Considerations

Camelids (Llamas and Alpacas)

  • Cases are acute in onset with rapid progression (often within 24-48 hours)
  • Seizures are more commonly reported in camelids than in other ruminants
  • Neonatal crias with failure of passive transfer may develop septicemic meningitis
  • Otitis media/interna may be an initial site of infection, progressing to CNS
  • Must differentiate from meningeal worm (Parelaphostrongylus tenuis) in endemic areas

Cervids (Deer Species)

  • Clinical illness documented in white-tailed deer, moose, roe deer, fallow deer
  • Septicemia more common than encephalitis in young cervids
  • Captive and farmed deer at higher risk due to silage feeding practices
  • Wild cervids may act as environmental reservoirs

Other Clinical Forms

Parameter Expected Finding Clinical Significance
Cell Count Mild to moderate pleocytosis (variable) Lower than typical bacterial meningitis
Cell Type Mononuclear/monocytic predominance (characteristic) Distinguishes from other bacterial infections
Protein Mildly to moderately elevated Indicates inflammation
Glucose Usually normal Helps differentiate from suppurative meningitis
Culture Often NEGATIVE (bacteria rarely in CSF) Negative culture does not rule out listeriosis

Diagnosis

Clinical Diagnosis

Presumptive diagnosis is based on the combination of characteristic asymmetric neurological signs and history of silage feeding. Key diagnostic criteria include:

  • Acute onset of unilateral cranial nerve deficits
  • Circling behavior (toward the affected side)
  • Facial paralysis with drooling and exposure keratitis
  • History of silage or poor-quality hay feeding
  • Winter-spring seasonality

Cerebrospinal Fluid Analysis

CSF analysis is highly useful for supporting a presumptive diagnosis of listeriosis:

High-YieldMONOCYTIC pleocytosis with NORMAL glucose is characteristic of listeriosis! This differs from other bacterial meningitis where neutrophils predominate and glucose is low. Remember: "Mono for Mono" - Monocytes for Listeria monocytogenes!

Confirmatory Diagnosis

Definitive diagnosis requires postmortem examination:

  • Histopathology: Pathognomonic findings include multifocal microabscesses in the brainstem (medulla oblongata and pons) with perivascular mononuclear cuffing, focal gliosis, and neuronal necrosis
  • Bacterial Culture: Isolation of L. monocytogenes from brainstem tissue (pons and trapezoid bodies are best)
  • PCR: Detection of L. monocytogenes DNA from brain tissue or CSF
  • Immunohistochemistry: Can detect listerial antigen in tissue sections

Differential Diagnosis

Condition Similar Features Differentiating Features
Meningeal Worm Neurologic signs in camelids; ataxia Hindlimb predominance; eosinophilia in CSF; no facial paralysis
Polioencephalomalacia Depression, circling, blindness Bilateral cortical blindness; responds to thiamine; no facial paralysis
Rabies Neurologic signs; behavioral changes No facial asymmetry; progressive paralysis; ALWAYS rule out
Brain Abscess Circling, neurologic deficits Contralateral blindness; no cranial nerve deficits; CT/MRI findings
Otitis Media/Interna Head tilt, nystagmus, facial paralysis Peripheral vestibular signs; normal mentation; may progress to listeriosis

Treatment

Antimicrobial Therapy

Early, aggressive antimicrobial therapy is essential for any chance of recovery. High doses are required to achieve adequate CNS penetration:

NAVLE TipCEPHALOSPORINS ARE INEFFECTIVE against Listeria! This is a critical point - never use ceftriaxone or other cephalosporins for suspected listeriosis. Remember: "C for Cephalosporin = C for Cannot treat Listeria!"

Supportive Care

  • Fluid Therapy: IV crystalloids for hydration; most patients cannot eat or drink
  • Anti-inflammatories: NSAIDs or corticosteroids (dexamethasone) for cerebral edema
  • Thiamine: 5-10 mg/kg (helps differentiate from PEM; not harmful if listeriosis)
  • Nutritional Support: Tube feeding if dysphagia present; rumen transfaunation in ruminants
  • Nursing Care: Frequent repositioning for recumbent animals; eye lubrication for exposure keratitis

Prognosis

Prognosis is guarded to poor for encephalitic listeriosis:

  • Case fatality rate: 50-70% in sheep/goats; approximately 50% in cattle; similar or higher in camelids
  • Recovery possible with early, aggressive treatment (within 24-48 hours of onset)
  • Negative prognostic indicators: Recumbency, severe dysphagia, absent menace response, excitement, seizures
  • Animals still ambulatory at presentation have better prognosis
  • Improvement usually seen within 3-5 days if treatment will be successful
  • Residual neurological deficits may persist in survivors
Drug Dosage Notes
Penicillin G (First-line) 22,000-44,000 IU/kg IV or IM q6-12h for 1-2 weeks minimum Start with potassium penicillin IV, transition to procaine penicillin IM
Oxytetracycline 16.5-20 mg/kg IV once daily for 5-7 days Alternative; good CNS penetration
Ampicillin 10-20 mg/kg IV q6-8h Human protocol; may add aminoglycoside

Prevention and Control

Feed Management

  • Silage pH: Ensure proper fermentation with pH less than 4.5 (Listeria cannot multiply below pH 5.0)
  • Avoid contamination: Minimize soil contamination during harvest
  • Discard spoiled feed: Do not feed moldy or aerobically deteriorated silage (top layer)
  • Clean feeding areas: Regularly clean feed bunks; remove leftover feed
  • Consider alternatives: For small camelid herds, avoid silage entirely if possible

Herd Management

  • Isolate affected animals immediately
  • Discontinue suspect silage if outbreak occurs
  • Quarantine new introductions
  • No effective vaccine currently available

Zoonotic Considerations

Listeriosis is a significant zoonotic disease. Important precautions include:

  • Wear gloves when handling affected animals, aborted fetuses, or placentas
  • Practice thorough hand hygiene
  • Pregnant women and immunocompromised individuals at highest risk
  • Do not consume raw milk from affected herds
  • Infected animals may not be slaughtered for human consumption

Exam Focus: Listeria is one of the "Big 4" foodborne zoonoses to remember: Listeria, Salmonella, E. coli O157:H7, and Campylobacter. High-risk groups for human listeriosis = "YOPI" - Young, Old, Pregnant, Immunocompromised.

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