Camelidae and Cervidae Endophyte Toxicity – NAVLE Study Guide

Overview and Clinical Importance

Endophyte toxicity represents a significant cause of neurological disease in grazing camelids and cervids. Endophytic fungi live symbiotically within certain pasture grasses, primarily tall fescue (Festuca arundinacea) and perennial ryegrass (Lolium perenne), producing mycotoxins that are beneficial to the plant but toxic to livestock. These toxicoses manifest as distinct clinical syndromes affecting the nervous system, thermoregulation, and peripheral circulation.

Camelids (llamas and alpacas) appear to be more susceptible to certain endophyte toxicoses than cattle or sheep, making recognition and prevention particularly important in camelid practice. Understanding endophyte toxicity is essential for NAVLE preparation as it encompasses toxicology, neurology, and herd health management principles.

Etiology and Pathophysiology

The Endophyte-Grass Relationship

Endophytes are fungi that live entirely within plant tissues without causing visible disease to the host plant. The relationship is mutualistic: the fungus receives nutrients and shelter, while the plant gains enhanced drought tolerance, insect resistance, and competitive advantage. Unfortunately, many alkaloids produced by these fungi are toxic to grazing mammals.

Key Endophyte Species and Host Grasses

Mechanisms of Toxicity

Lolitrem B (Ryegrass Staggers)

Lolitrem B is an indole-diterpene alkaloid that acts as a potent BK channel blocker (large-conductance calcium-activated potassium channels). These channels are critical for regulating neuronal excitability and neurotransmitter release. Blockade results in:

• Increased neuronal excitability leading to tremors
• Disrupted motor coordination causing ataxia
• Effects are reversible once toxin exposure ceases
• Lolitrem B is lipophilic and stored in fat, causing slow onset and prolonged effects

Ergovaline (Fescue Toxicosis)

Ergovaline is an ergopeptine alkaloid that acts as a dopamine D2 receptor agonist and causes peripheral vasoconstriction. Key effects include:

• Inhibition of prolactin release (causes agalactia)
• Peripheral vasoconstriction (causes gangrene of extremities in cold weather)
• Impaired thermoregulation (heat intolerance in summer)
• Reproductive dysfunction (prolonged gestation, thickened placentas)

Toxin Threshold Concentrations

Clinical Syndromes

Ryegrass Staggers

Ryegrass staggers is most commonly reported in Australia and New Zealand, but sporadic cases occur in Europe and the Americas. Camelids appear to be highly susceptible, with alpacas under 2 years of age most commonly affected. The disease typically occurs in mid to late summer and autumn or after drought when new grass growth emerges.

Clinical Signs in Camelids

• Head and neck tremors - most characteristic sign in alpacas
• Fine muscle tremors that worsen with excitement or exercise
• Ataxia with stiff, stilted gait (sawhorse stance)
• Hypermetria (exaggerated movements)
• Collapse when startled or forced to move quickly
• Normal mentation between episodes
• Signs appear at rest but dramatically worsen with activity

Fescue Toxicosis

Fescue toxicosis encompasses several clinical syndromes caused by ergot alkaloids, primarily ergovaline, from endophyte-infected tall fescue. Tall fescue covers over 40 million acres in the United States, predominantly in the transition zone. The syndrome manifests differently depending on season and duration of exposure.

Fescue Toxicosis Clinical Syndromes

Species Susceptibility

Diagnosis

Diagnosis of endophyte toxicity is primarily clinical and circumstantial, based on history, clinical signs, pasture evaluation, and response to removal from toxic pasture.

Diagnostic Approach

History and Physical Examination

• Access to perennial ryegrass or tall fescue pastures
• Season (late summer/autumn for staggers; any season for fescue)
• Multiple animals affected in a herd/flock
• Neurological examination: tremors worsen with stimulation (staggers)
• Peripheral examination: cold extremities, line of demarcation (fescue foot)

Laboratory and Forage Testing

Differential Diagnosis

Neurological signs in camelids and cervids have multiple potential causes. Key differentials for endophyte toxicity include:

Treatment

There is no specific antidote for endophyte toxicity. Treatment is primarily supportive and involves removal from toxic pasture.

Treatment Protocol

Prevention and Management

Pasture Management Strategies

• Test pastures for endophyte infection - identify percentage of infected plants
• Dilute infected fescue with legumes - clover, alfalfa reduce overall toxin intake
• Avoid grazing during high-risk periods - late summer/autumn for staggers; seed head formation for fescue
• Maintain grazing height - toxins concentrated in lower plant/crowns; avoid overgrazing
• Clip seed heads - highest toxin concentration in seed heads
• Reseed with novel endophyte or endophyte-free varieties - long-term solution but expensive
• Avoid high nitrogen fertilization - increases ergovaline production
• Stockpiled fescue in late fall/winter is safer - toxin levels decline with frost

Novel Endophyte Varieties

Plant breeders have developed grass varieties infected with novel or friendly endophytes that provide pest resistance without producing harmful alkaloids. These include:

• AR1 - produces peramine (insect deterrent) but no lolitrem B or ergovaline
• AR37 - produces small amounts of janthitrems; excellent pest resistance
• MaxQ (tall fescue) - novel endophyte fescue with no ergovaline production

Prognosis