5.2 Ovine, Caprine & Camelid Medicine & Management

Small Ruminant & Camelid Medicine

Small ruminants (sheep and goats) and camelids (llamas and alpacas) share several management and medical challenges, particularly regarding parasitism and metabolic diseases. However, they possess distinct species-specific physiological and pathological responses that are highly tested on the NAVLE.

Parasite Management & FAMACHA Scoring

The most economically significant internal parasite of sheep and goats is Haemonchus contortus, commonly known as the Barber's Pole Worm. This blood-feeding nematode resides in the abomasum, where it pierces the mucosa to ingest blood. Heavy infections cause regenerative anemia, hypoproteinemia, and severe lethargy. Because it causes a loss of blood rather than intestinal inflammation, infected small ruminants do not typically present with diarrhea. Instead, they present with submandibular edema (bottle jaw) due to hypoalbuminemia.

To combat widespread anthelmintic resistance, veterinarians and producers use the FAMACHA eye scoring system. This clinical tool evaluates the color of the lower eyelid conjunctiva against a color chart to estimate the degree of anemia:

• Score 1 (Red): Optimal, non-anemic. No treatment.
• Score 2 (Pink-Red): Acceptable. No treatment.
• Score 3 (Pink): Borderline. Treat selectively based on body condition score, age, lactation status, or history.
• Score 4 (Pink-White): Anemic. Treatment required.
• Score 5 (White): Severely anemic. Immediate treatment and supportive care required.

This targeted treatment strategy preserves a population of parasites in refugia (worms not exposed to the anthelmintic). By keeping a pool of susceptible genes in the environment, the development of multi-drug resistance to benzimidazoles (e.g., fenbendazole), macrocyclic lactones (e.g., moxidectin), and imidazothiazoles (e.g., levamisole) is significantly slowed.

Metabolic & Infectious Diseases of Small Ruminants

Pregnancy Toxemia (Twin Lamb Disease)

Pregnancy toxemia is a metabolic disorder occurring in late gestation (last 2-4 weeks) in ewes and does carrying multiple fetuses (twins, triplets). The physical size of the pregnant uterus compresses the rumen, reducing the animal's capacity for feed intake at a time when energy demands are at their peak. This leads to a severe negative energy balance. The animal mobilizes fat reserves, resulting in hepatic lipidosis, hyperketonemia, and metabolic acidosis.

• Clinical Signs: Initial separation from the flock, depression, blindness (due to hypoglycemic encephalopathy), muscle tremors of the muzzle, progressive recumbency, and death.
• Diagnostics: Hypoglycemia (early), elevated blood beta-hydroxybutyrate (BHBA > 1.6 mmol/L), metabolic acidosis, and ketonuria.
• Treatment: Mild cases are treated with oral propylene glycol (100-200 mL, BID) and high-energy supplements. Recumbent animals require intravenous dextrose (50% solution), correction of metabolic acidosis with sodium bicarbonate, and immediate delivery of the fetuses via C-section or induction of parturition (using dexamethasone in ewes, or prostaglandin F2-alpha and dexamethasone in does).

Caseous Lymphadenitis (CLA)

CLA is a chronic, contagious disease caused by Corynebacterium pseudotuberculosis, a Gram-positive, facultative intracellular bacterium. It enters the body through skin wounds (e.g., shearing, head-butting, tagging).

• Clinical Signs: Suppurative necrotizing lymphadenitis. Abscesses form in external lymph nodes (parotid, submandibular, prescapular, prefemoral), containing a thick, odorless, cheesy green-yellow pus. In sheep, these abscesses develop a classic concentric, laminated "onion-skin" pattern. The internal form causes abscessation of the lungs, mediastinal lymph nodes, and kidneys, presenting as chronic weight loss ("thin ewe syndrome").
• Control: The intracellular nature of the pathogen and the thick capsule of the abscesses make antibiotic treatment ineffective. Abscesses should not be lanced in the main pen, as the discharge highly contaminates the environment. The primary control strategy is isolation and culling of affected animals, maintaining strict hygiene during shearing, and vaccination (which reduces the number and severity of abscesses but does not prevent infection).

Contagious Ecthyma (Soremouth / Orf)

Contagious ecthyma is caused by a parapoxvirus that is highly resistant in the environment. It is zoonotic, causing painful crusting lesions on the hands of handlers. In small ruminants, it causes proliferative, thick scabs on the lips, muzzle, and nostrils. These lesions can spread to the teats of dams nursing infected lambs, causing severe pain that leads to refusal to nurse and secondary mastitis. The disease is self-limiting and resolves in 3-4 weeks. Supportive care is indicated. A live, virulent vaccine is available but should only be used in herds with confirmed endemic infections, applied via scarification of the skin.

Camelid-Specific Conditions

Meningeal Worm (Paralaphostrongylus tenuis)

Also known as the brainworm, Paralaphostrongylus tenuis is a parasite of the meninges of the white-tailed deer (Odocoileus virginianus). Camelids (llamas and alpacas) are aberrant, dead-end hosts. They ingest terrestrial snails or slugs containing infective L3 larvae on pasture. The larvae migrate out of the gastrointestinal tract and enter the spinal cord and brain, causing severe cerebrospinal nematodiasis.

• Clinical Signs: Asymmetric ataxia, hindlimb weakness, hypermetria, proprioceptive deficits, head tilt, and eventual recumbency.
• Diagnostics: Cerebrospinal fluid (CSF) tap reveals eosinophilic pleocytosis (elevated WBCs with >10% eosinophils) and elevated protein. Definite diagnosis is confirmed via histopathology of the brain/spinal cord at necropsy.
• Treatment: Aggressive therapy must begin immediately. High-dose fenbendazole (50 mg/kg, orally for 5 days) is used as it crosses the blood-brain barrier. Concurrent anti-inflammatory therapy (e.g., flunixin meglumine or dexamethasone) is critical to suppress the severe inflammatory reaction caused by dying larvae. The prognosis is guarded to poor once recumbency occurs.

Hepatic Lipidosis in Camelids

Camelids have unique energy metabolism and are highly susceptible to hepatic lipidosis when subjected to stressors, systemic illness, or gestation/lactation. A negative energy balance triggers rapid, massive mobilization of non-esterified fatty acids (NEFAs) from adipose tissue. The liver is quickly overwhelmed, leading to diffuse lipid accumulation in hepatocytes.

• Clinical Signs: Anorexia, depression, weakness, recumbency, and signs of hepatic encephalopathy.
• Diagnostics: Elevated liver enzymes (GGT, AST, SDH), high serum bile acids, hypertriglyceridemia, and varying blood glucose levels.
• Treatment: Early aggressive nutritional support. Tube feeding with camelid-specific slurries, intravenous dextrose infusions, amino acid supplementation, and insulin therapy to suppress lipolysis. The underlying cause must be identified and corrected.