3.3 Equine Common Infectious & Non-Infectious Diseases

Equine Common Infectious & Non-Infectious Diseases

Veterinarians must identify, diagnose, and manage a wide range of infectious and non-infectious conditions. Many of these diseases have strict regulatory requirements, complex pathophysiologies, or require specific long-term management.

Equine Infectious Anemia (EIA)

Equine Infectious Anemia (EIA) is a persistent, blood-borne viral disease of equids caused by a lentivirus (family Retroviridae).

• Transmission: Mechanically transmitted by biting flies, particularly horse flies (family Tabanidae) and deer flies (family Chrysops), which transfer infective blood on their mouthparts. It is also spread via contaminated needles, surgical instruments, or blood transfusions.
• Pathogenesis: The virus infects macrophages, leading to persistent infection and cycles of viremia. Clinical signs result from immune-mediated destruction of red blood cells and platelets.
• Clinical Signs:
  • Acute: High fever, severe depression, thrombocytopenia, petechial hemorrhages, and anemia.
  • Chronic (Swamp Fever): Recurrent cycles of fever, weight loss, cachexia, ventral edema, and anemia.
  • Inapparent carrier: The most common form; horses show no clinical signs but remain viremic for life and act as a reservoir.
• Diagnosis: The Coggins test (agar gel immunodiffusion, AGID) is the gold standard diagnostic and regulatory test. ELISA tests are used for rapid screening, but any positive ELISA must be confirmed by the AGID test due to potential false positives.
• Management and Regulations: There is no treatment or vaccine. Confirmed positive horses must be permanently isolated (minimum of 200 yards from any other equids) or euthanized. Federal and state laws regulate movement and require negative Coggins certificates for transport or show.

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Strangles (Streptococcus equi subsp. equi)

Strangles is a highly contagious upper respiratory tract infection of equids caused by Streptococcus equi subsp. equi, a Gram-positive, beta-hemolytic, encapsulated bacterium.

• Transmission: Occurs via direct contact with nasal secretions or abscess fluid from infected horses, or indirectly via contaminated fomites (water troughs, grooming equipment, pasture gates).
• Clinical Signs: Acute onset of fever, bilateral mucopurulent nasal discharge, and painful lymphadenomegaly (primarily submandibular and retropharyngeal lymph nodes) that progresses to abscessation and rupture. Compression of the larynx/trachea by enlarged lymph nodes can cause dyspnea and dysphagia.
• Complications:
  • Bastard Strangles: Metastatic spread of infection to internal lymph nodes (e.g., mesenteric, mediastinal) or organs. Signs include chronic weight loss, recurrent colic, or fever.
  • Purpura Hemorrhagica: A Type III hypersensitivity reaction causing aseptic necrotizing vasculitis due to deposition of antigen-antibody (IgG-S. equi protein) complexes in vessel walls. Signs include severe, cold, well-demarcated ventral and limb edema, petechiae, ecchymoses, and stiffness.
  • Guttural Pouch Empyema & Chondroids: Accumulation of purulent exudate in the guttural pouches. When the pus dries, it forms solid, egg-shaped concretions called chondroids. Horses with chondroids become chronic, asymptomatic carriers that shed the bacteria.
• Diagnosis: PCR or bacterial culture of nasal swabs, nasal washes, or guttural pouch lavages.
• Treatment: Strict biosecurity and quarantine. For uncomplicated cases, supportive care (warm compresses to abscesses to promote drainage) is recommended. Antibiotics (penicillin) are controversial: they are indicated in dyspneic horses, purpura hemorrhagica (along with dexamethasone), or guttural pouch empyema, but contraindicated in uncomplicated active abscesses because they delay abscess maturation and prolong the disease course.

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Equine Herpesvirus (EHV-1 & EHV-4)

EHV-1 and EHV-4 are major herpesviruses of horses. While they share genetic similarities, their clinical syndromes differ:

• EHV-4: Primarily causes respiratory disease (equine rhinopneumonitis) in young horses, characterized by fever, serous to mucopurulent nasal discharge, and coughing. It rarely causes abortion or neurological signs.
• EHV-1: A more pathogenic strain that causes respiratory disease, late-term abortion ("abortion storms" at 7–11 months of gestation), neonatal mortality, and Equine Herpesvirus Myeloencephalopathy (EHM).
• EHM Pathogenesis: Neuropathogenic strains of EHV-1 cause endothelial cell infection, vasculitis, thrombosis, and ischemic necrosis within the spinal cord and brain microvasculature. It is not a direct infection of neurons.
• Clinical Signs of EHM: Sudden onset of symmetric hindlimb ataxia, weakness, hypotonic tail and anus, and urinary incontinence (urine dribbling).
• Diagnosis: PCR of nasal swabs and EDTA blood (buffy coat).
• Prevention: Biosecurity and vaccination. Vaccines protect against respiratory disease and abortion but are not labeled to protect against EHM.

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Laminitis

Laminitis is the painful inflammation and failure of the digital laminae that secure the third phalanx (P3 or coffin bone) to the hoof wall, leading to P3 rotation or sinking.

• Etiologies:
  • Systemic Inflammatory Response Syndrome (SIRS): Endotoxemia from colitis, grain overload, or retained placenta (metritis).
  • Endocrinopathy: Insulin dysregulation associated with PPID or Equine Metabolic Syndrome (EMS).
  • Supporting limb laminitis: Mechanical overload of the contralateral limb due to non-weight-bearing lameness.
• Signs: "Sawhorse stance" (shifting weight backward onto the heels), bounding digital pulses, warm hoof walls, pain on hoof tester pressure at the toe.
• Treatment: Cryotherapy (immersion of distal limbs in ice-water slurry) is highly protective if applied during the developmental phase. NSAIDs (flunixin meglumine or firocoxib) for pain control. Supportive shoeing (styrofoam pads, wooden shoes) and deep bedding. Restriction of non-structural carbohydrates in endocrine cases.

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Pituitary Pars Intermedia Dysfunction (PPID / Cushing's)

PPID is a common neurodegenerative disease of older horses (>15 years).

• Pathogenesis: Loss of dopaminergic neurons in the hypothalamus leads to loss of inhibitory control over the pituitary pars intermedia, resulting in hyperplasia and hypersecretion of ACTH, POMC, and other peptides.
• Signs: Hypertrichosis (long, curly hair coat that fails to shed), muscle wasting (especially epaxial muscles), cresty neck, supraorbital fat pads, polyuria/polydipsia, and recurrent laminitis.
• Diagnostics: Resting plasma ACTH concentration (reference ranges must adjust for the autumn rise). The TRH stimulation test is the gold standard for early cases (measuring ACTH 10 minutes post-TRH).
• Treatment: Pergolide (dopamine agonist) administered daily.

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Recurrent Exertional Rhabdomyolysis (RER)

RER is an autosomal dominant disorder of intracellular calcium regulation in skeletal muscle, triggered by exercise, excitement, and high-starch diets. It primarily affects Thoroughbreds, Standardbreds, and Arabians.

• Signs: Muscle cramping, stiffness, sweating, tachypnea, reluctance to move ("tying up"), and myoglobinuria (reddish-brown urine).
• Diagnostics: Clinical signs and marked elevation in serum creatine kinase (CK) and aspartate aminotransferase (AST).
• Treatment: Rest, sedation (acepromazine or detomidine), NSAIDs (only when hydrated to avoid renal toxicity), fluid therapy to prevent acute renal failure from myoglobinuria. Long-term management requires a low-starch, high-fat diet.