Guttural Pouch Mycosis
Basic Information
Clinical Presentation
Physical Exam Findings
• Acute, moderate to severe epistaxis:
• Tachycardia, tachypnea, pale mucous membranes, weak peripheral pulses, anxious demeanor, weakness
• The inability to blink may lead to the development of corneal ulcers on the affected side.
• Other less common clinical signs: Nasal discharge, colic, blindness, unusual head carriage, parotid area pain, head shyness.
Etiology and Pathophysiology
• The most common etiologic agents recovered from horses with guttural pouch mycosis are Emericella nidulans and Aspergillus fumigatus.
• These fungi are ubiquitous and thrive in warm, moist areas such as bedding material containing urine and water.
• These fungi act as opportunistic pathogens, entering the guttural pouch through the pharyngeal orifice, where they incite an inflammatory response.
• This leads to the formation of a diphtheritic membrane, composed of necrotic tissue, cell debris, bacteria, and fungal mycelia.
• The fungi can penetrate deeper tissues, causing thromboarteritis, aneurysm, and hemorrhage.
• Damage may occur to any of the nerves within the guttural pouch because of the acute inflammatory response or because of chronic fibrosis.
Diagnosis
Differential Diagnosis
Initial Database
• Complete blood count: Normal
• Hematocrit: Normal in the acute stages (<24 hours after hemorrhage); decreased later
• Total protein: Normal in the subacute stages (<4–6 hours after hemorrhage); decreased later
• Fibrinogen: Normal, decreased (if substantial hemorrhage), or increased (chronic inflammation or infection)
• Platelet count: Normal or decreased after substantial hemorrhage
• Serum chemistry: Normal or azotemia (prerenal) if hypovolemic shock is present
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