Guttural Pouch Mycosis and Empyema

Guttural pouch mycosis (GPM) and guttural pouch empyema (GPE) are distinct clinical entities affecting the equine guttural pouch, a unique diverticulum of the Eustachian tube. GPM is a fungal infection, most commonly caused by Aspergillus spp., that invades the mucosa and submucosa, often eroding the internal carotid artery, external carotid artery, or maxillary artery, leading to fatal hemorrhage. GPE is a bacterial infection characterized by the accumulation of purulent exudate within the pouch, often secondary to upper respiratory infections or guttural pouch tympany. Both conditions are clinically significant in performance horses, particularly those involved in racing, dressage, and eventing, due to their impact on upper airway function and the potential for life-threatening complications. The guttural pouch is a paired, air-filled sac located in the parotid region, communicating with the nasopharynx via the pharyngeal orifice. It has a capacity of approximately 300-500 mL in adult horses and is intimately associated with several cranial nerves (IX, X, XI, XII) and the sympathetic trunk, making it a critical anatomical site for neurological deficits. GPM is more prevalent in horses aged 2-10 years, with no breed predilection, while GPE is more common in younger horses, especially those with conformational abnormalities of the guttural pouch openings. Both conditions require prompt diagnosis and aggressive management to prevent severe morbidity and mortality.

Guttural pouch mycosis is primarily caused by opportunistic fungi, with Aspergillus fumigatus being the most frequently isolated species, followed by Aspergillus niger and other saprophytic molds. These fungi are ubiquitous in the environment, particularly in hay, straw, and soil, and typically do not cause disease in immunocompetent horses. However, factors such as stress, concurrent immunosuppression, or local tissue damage may predispose to fungal colonization and invasion. The fungus invades the mucosal lining, often at the level of the internal carotid artery, where it forms a mycotic plaque that can erode the arterial wall, leading to aneurysm formation and rupture. Guttural pouch empyema is most commonly caused by Streptococcus equi subsp. equi (the causative agent of strangles), but other bacteria such as Streptococcus zooepidemicus, Pasteurella spp., and anaerobic organisms may also be involved. GPE often arises as a complication of upper respiratory tract infections, guttural pouch tympany, or foreign body penetration. The accumulation of purulent material can lead to chondroid formation (inspissated pus) and chronic inflammation, which may cause neurological deficits due to compression of adjacent nerves.

Guttural pouch mycosis is relatively uncommon but can affect horses of any breed, age, or sex, with a slight predilection for horses aged 2-10 years. There is no strong breed or sex predisposition, but horses housed in environments with high fungal spore exposure, such as dusty stables or those fed moldy hay, may be at increased risk. GPE is more common in young horses, particularly foals and yearlings, and is frequently associated with outbreaks of strangles. Horses with poor guttural pouch drainage due to conformational abnormalities, such as a narrow pharyngeal orifice or excessive soft palate length, are predisposed. The incidence of GPE has decreased with improved vaccination and management practices for strangles, but it remains a significant cause of morbidity in weanlings and yearlings. Both conditions can have a substantial impact on athletic performance, with GPM carrying a high mortality rate (up to 50%) due to fatal hemorrhage, while GPE can lead to chronic nasal discharge, respiratory noise, and neurological deficits if left untreated.

In guttural pouch mycosis, the fungal hyphae invade the mucosal epithelium and submucosa, causing necrosis and inflammation. The fungus has a predilection for the arterial walls, particularly the internal carotid artery, where it causes mycotic arteritis. The inflammatory response leads to weakening of the arterial wall, aneurysm formation, and eventual rupture, resulting in massive epistaxis. The fungus may also extend to involve the facial nerve, glossopharyngeal nerve, vagus nerve, and sympathetic trunk, leading to dysphagia, laryngeal hemiplegia, Horner's syndrome, and other neurological deficits. In guttural pouch empyema, bacterial infection causes an acute inflammatory response with neutrophil infiltration, leading to the accumulation of purulent exudate. If the infection is not resolved, the exudate may become inspissated, forming chondroids that can obstruct the pouch and cause chronic inflammation. The inflammatory process can also affect adjacent nerves, leading to similar neurological signs as GPM, although less commonly. In both conditions, the guttural pouch's unique anatomy, with its close proximity to major arteries and nerves, predisposes to severe complications.

Intrinsic risk factors for guttural pouch mycosis include age (2-10 years), individual susceptibility to fungal infection, and possibly genetic factors affecting immune response. Extrinsic factors include exposure to moldy feed or bedding, poor ventilation in stables, and high environmental fungal spore counts. For guttural pouch empyema, intrinsic factors include young age (foals and yearlings), conformational abnormalities of the guttural pouch openings, and immunodeficiency. Extrinsic factors include exposure to Streptococcus equi, poor biosecurity, and stress from transportation or weaning. Additionally, horses that have had guttural pouch tympany or previous upper respiratory infections are at increased risk for GPE. Management practices such as overcrowding, poor hygiene, and lack of vaccination against strangles can also contribute to the development of GPE.

Guttural pouch mycosis often presents with sudden, profuse, and often fatal epistaxis due to arterial rupture. Prior to hemorrhage, horses may show no clinical signs or may have a history of intermittent, mild epistaxis, nasal discharge, or dysphagia. Neurological signs may include dysphagia, laryngeal hemiplegia (roaring), Horner's syndrome (ptosis, miosis, enophthalmos, sweating on the affected side of the face), and facial nerve paralysis (ear droop, lip droop). Guttural pouch empyema typically presents with bilateral or unilateral purulent nasal discharge, which may be intermittent and worse during exercise or when the head is lowered. Horses may also have a foul odor from the mouth or nose, fever, depression, and anorexia. In chronic cases, chondroids may form, leading to persistent nasal discharge and respiratory noise. Neurological signs are less common but can occur if the infection spreads to adjacent nerves. Physical examination may reveal swelling in the parotid region, pain on palpation, and enlarged retropharyngeal lymph nodes.

Differential diagnoses for guttural pouch mycosis include: 1) Guttural pouch empyema, which typically presents with purulent nasal discharge and fever, and is diagnosed via endoscopy showing purulent material or chondroids. 2) Guttural pouch tympany, which occurs in foals and presents with a characteristic non-painful swelling in the parotid region, and is diagnosed by endoscopy showing air-filled pouch. 3) Upper respiratory tract infections (e.g., strangles, influenza) that may cause secondary guttural pouch involvement. 4) Dental disease or sinusitis, which can cause nasal discharge and facial swelling. 5) Neoplasia (e.g., lymphoma, squamous cell carcinoma) of the guttural pouch, which is rare but can cause similar signs. 6) Trauma to the head or neck, which can cause hemorrhage or neurological deficits. For guttural pouch empyema, differentials include: 1) Guttural pouch mycosis, which may present with epistaxis and neurological signs. 2) Guttural pouch tympany, which is more common in foals and presents with a non-painful swelling. 3) Sinusitis, which can cause unilateral nasal discharge and facial swelling. 4) Dental disease, which can cause purulent nasal discharge. 5) Strangles, which is a primary cause of guttural pouch empyema. 6) Foreign body in the guttural pouch, which is rare but can cause similar signs.

The diagnostic approach for guttural pouch mycosis and empyema begins with a thorough history and physical examination, including assessment of the respiratory tract and neurological status. If guttural pouch disease is suspected, the next step is endoscopic examination of the upper airway, including the guttural pouch. Endoscopy allows direct visualization of the pouch, revealing fungal plaques, hemorrhage, or purulent material. For GPM, endoscopy may show a characteristic white to yellow fungal plaque, often overlying the internal carotid artery. For GPE, endoscopy may show purulent exudate, chondroids, or inflammation of the pouch lining. If hemorrhage is suspected, a complete blood count and coagulation profile should be performed. Radiography of the guttural pouch may be useful to identify chondroids or fluid lines, but is less sensitive than endoscopy. Ultrasonography can be used to assess the carotid arteries for aneurysm or thrombosis. In cases of suspected arterial involvement, angiography or CT angiography may be performed to identify the affected artery and plan surgical intervention. For GPE, bacterial culture and sensitivity of the purulent material should be obtained to guide antimicrobial therapy. In all cases, a neurological examination should be performed to assess for cranial nerve deficits.

In guttural pouch mycosis, laboratory findings may be unremarkable unless there has been significant hemorrhage, in which case anemia (decreased packed cell volume, hemoglobin) may be present. In guttural pouch empyema, a complete blood count may reveal leukocytosis with neutrophilia and hyperfibrinogenemia due to bacterial infection. Serum amyloid A (SAA) may be elevated. Bacterial culture of the purulent exudate may yield Streptococcus equi or other bacteria. In chronic cases, hyperglobulinemia may be present. If neurological signs are present, cerebrospinal fluid analysis may be normal or show mild inflammation. In cases of guttural pouch mycosis, fungal culture of the plaque may be attempted but is often unrewarding. Coagulation profiles may be normal unless there is disseminated intravascular coagulation secondary to severe hemorrhage.

Endoscopy is the primary imaging modality for guttural pouch disease. In GPM, endoscopy reveals a fungal plaque, often with hemorrhage or erosion of the arterial wall. In GPE, endoscopy shows purulent exudate, chondroids, or mucosal inflammation. Radiography of the guttural pouch may show a fluid line or soft tissue opacity in cases of empyema, and may reveal chondroids as mineralized opacities. Ultrasonography of the parotid region can be used to assess the carotid arteries for aneurysm, thrombosis, or perivascular fluid. CT angiography is the gold standard for evaluating the arterial supply to the guttural pouch and can precisely identify the affected artery, which is crucial for surgical planning. MRI may be useful for assessing soft tissue involvement and neurological complications. Scintigraphy is not commonly used for guttural pouch disease but may be helpful in cases of chronic inflammation.

Cytological examination of guttural pouch exudate in GPE typically reveals degenerate neutrophils, bacteria, and cellular debris. Fungal hyphae may be seen in GPM if the plaque is sampled. Histopathology of the guttural pouch mucosa in GPM shows fungal hyphae invading the submucosa, with necrosis, thrombosis, and arteritis. In GPE, histopathology shows chronic inflammation, fibrosis, and possibly chondroid formation. Biopsy of the guttural pouch lining may be performed during endoscopy, but is rarely necessary for diagnosis.

Treatment of guttural pouch mycosis is primarily surgical, aimed at preventing fatal hemorrhage. The most common surgical technique is balloon-tipped catheter occlusion of the affected artery (internal carotid, external carotid, or maxillary artery) proximal and distal to the mycotic lesion. This procedure is performed under general anesthesia and involves placing catheters via a transarterial approach. Alternatively, arterial ligation may be performed. Postoperative care includes antimicrobial therapy (e.g., penicillin, gentamicin) and anti-inflammatory drugs (e.g., flunixin meglumine). Topical antifungal therapy (e.g., enilconazole or miconazole) may be infused into the pouch via a catheter, but systemic antifungals are generally not effective. In cases of guttural pouch empyema, treatment involves drainage of the pouch, which can be achieved by repeated endoscopic lavage with warm saline or by surgical drainage via a modified Whitehouse approach. Systemic antimicrobial therapy should be based on culture and sensitivity, with penicillin being the drug of choice for Streptococcus equi. Non-steroidal anti-inflammatory drugs (e.g., flunixin meglumine) are used to reduce inflammation and fever. In chronic cases with chondroids, surgical removal may be necessary. Supportive care includes nutritional support if dysphagia is present, and management of neurological deficits.

The prognosis for guttural pouch mycosis is guarded to poor, with a high mortality rate (up to 50%) due to fatal hemorrhage. If the horse survives the initial hemorrhage and undergoes successful surgical occlusion of the affected artery, the prognosis for life is good, but the prognosis for return to athletic function depends on the presence and severity of neurological deficits. Dysphagia and laryngeal hemiplegia can significantly impair performance. The prognosis for guttural pouch empyema is generally good with appropriate treatment, especially if diagnosed early. Most horses respond to drainage and antimicrobial therapy, with resolution of clinical signs within 2-4 weeks. However, chronic cases with chondroids may have a more guarded prognosis, and neurological complications can occur. Recurrence is possible if the underlying cause is not addressed.

After treatment for guttural pouch mycosis, horses should be monitored closely for signs of hemorrhage, neurological deficits, and infection. Serial endoscopic examinations are recommended to assess healing of the pouch and to monitor for recurrence. Horses that have undergone arterial occlusion should have regular ultrasound or CT evaluation of the affected artery. For guttural pouch empyema, follow-up endoscopy is recommended to ensure complete resolution of the infection and to check for chondroid formation. Horses should be rested from exercise for at least 2-4 weeks after treatment, and gradually returned to work. If neurological deficits are present, a longer rehabilitation period may be necessary. Regular veterinary check-ups are essential to monitor for complications.

Clinical pearls: 1) Any horse with sudden, profuse epistaxis should be suspected of guttural pouch mycosis until proven otherwise. 2) Endoscopy of the guttural pouch is essential for diagnosis and should be performed in any horse with unexplained nasal discharge or neurological signs. 3) In cases of guttural pouch empyema, culture and sensitivity of the exudate is crucial for appropriate antimicrobial therapy. 4) Surgical occlusion of the affected artery is the definitive treatment for guttural pouch mycosis and should be performed as soon as possible to prevent fatal hemorrhage. Pitfalls: 1) Failure to perform endoscopy in horses with epistaxis can lead to misdiagnosis and death. 2) In guttural pouch empyema, relying solely on systemic antimicrobials without drainage may lead to chronic infection and chondroid formation. 3) In guttural pouch mycosis, attempting to biopsy the fungal plaque can precipitate fatal hemorrhage. 4) Overlooking neurological deficits can lead to poor outcomes, as they may be irreversible.

For guttural pouch mycosis, topical antifungal therapy may be administered via a catheter placed into the pouch. Enilconazole (1% solution) or miconazole (1% solution) can be infused at a dose of 100-200 mL per pouch, once daily for 7-14 days. Systemic antifungals such as itraconazole (5 mg/kg PO q24h) or fluconazole (14 mg/kg PO q24h) are not consistently effective but may be used in some cases. For guttural pouch empyema, antimicrobial therapy should be based on culture and sensitivity. Penicillin G (22,000 IU/kg IV q6h or 44,000 IU/kg IM q12h) is the drug of choice for Streptococcus equi. Gentamicin (6.6 mg/kg IV q24h) may be added for broad-spectrum coverage. Flunixin meglumine (1.1 mg/kg IV or PO q12h) is used for anti-inflammatory and analgesic effects. In cases of severe inflammation, dexamethasone (0.05-0.1 mg/kg IV q24h) may be used for 1-2 days. For supportive care, intravenous fluids (e.g., lactated Ringer's solution) may be administered at maintenance rates (50-60 mL/kg/day).

Evidence-based literature on guttural pouch mycosis and empyema is limited to retrospective studies and case series. A landmark study by Freeman et al. (1993) described the surgical management of guttural pouch mycosis using balloon-tipped catheters, reporting a survival rate of 80% in horses that underwent surgery. A more recent study by Perkins et al. (2006) evaluated the long-term outcome of horses with guttural pouch mycosis, finding that 60% of horses returned to their previous level of athletic activity after successful surgery. For guttural pouch empyema, a study by Judy et al. (1999) reported that endoscopic lavage and systemic antimicrobial therapy were effective in resolving clinical signs in 85% of cases. The ACVIM consensus statement on respiratory diseases in horses (2015) recommends early endoscopic evaluation and aggressive treatment for guttural pouch diseases. Overall, the evidence supports surgical intervention for guttural pouch mycosis to prevent fatal hemorrhage, and a combination of drainage and antimicrobial therapy for guttural pouch empyema.