Diseases of the upper respiratory tract
Rhinitis (inflammation of the nasal mucosa) is characterized clinically by sneezing, wheezing, and stertor during inspiration and a nasal discharge that may be serous, mucoid, or purulent in consistency depending on the cause.
Rhinitis usually occurs in conjunction with inflammation of other parts of the respiratory tract. It is present as a minor lesion in most bacterial and viral pneumonias but the diseases listed are those in which it occurs as an obvious and important part of the syndrome.
• Catarrhal rhinitis in infectious bovine rhinotracheitis, adenoviruses 1, 2 and 3 and respiratory syncytial virus infections
• Ulcerative/erosive rhinitis in bovine malignant catarrh, mucosal disease, rinderpest
• Rhinosporidiosis caused by fungi, the blood fluke Schistosoma nasalis and the supposedly allergic ‘summer snuffles’ also known as atopic rhinitis1
• Familial allergic rhinitis in cattle in which the progeny of affected cows are susceptible to allergic rhinitis2
• Bovine nasal eosinophilic granuloma due to Nocardia sp.3
• Glanders, strangles, and epizootic lymphangitis
• Infections with the viruses of equine viral rhinopneumonitis (herpesvirus-1), equine viral arteritis, influenza H3N8 equine rhinovirus, parainfluenza virus, reovirus, adenovirus
• Chronic rhinitis claimed to be caused by dust in dusty stables, and acute rhinitis occurring after inhalation of smoke and fumes
• Nasal granulomas due to chronic infections with Pseudoallescheria boydii4 and Aspergillus, Conidiobolus and Mucoraceous fungi5
• Equine grass sickness (dysautonomia, pp 1988–1990) in the chronic form causes rhinitis sicca.
• Melioidosis, bluetongue, rarely contagious ecthyma and sheep pox
• Oestrus ovis and Elaeophora schneideri infestations
• Purulent rhinitis and otitis associated with P. aeruginosa in sheep showered with contaminated wash.6
Rhinitis is of minor importance as a disease process except in severe cases when it causes obstruction of the passage of air through the nasal cavities. Its major importance is as an indication of the presence of some specific diseases. The type of lesion produced is important. The erosive and ulcerative lesions of rinderpest, bovine malignant catarrh and mucosal disease, the ulcerative lesions of glanders, melioidosis, and epizootic lymphangitis and the granular rhinitis of the anterior nares in allergic rhinitis all have diagnostic significance.
In atrophic rhinitis of pigs the destruction of the turbinate bones and distortion of the face appear to be a form of devitalization and atrophy of bone caused by a primary, inflammatory rhinitis. Secondary bacterial invasion of facial tissue of swine appears to be the basis of necrotic rhinitis.
The primary clinical finding in rhinitis is a nasal discharge, which is usually serous initially but soon becomes mucoid and, in bacterial infections, purulent. Erythema, erosion, or ulceration may be visible on inspection. The inflammation may be unilateral or bilateral. Sneezing is characteristic in the early acute stages and this is followed in the later stages by snorting and the expulsion of large amounts of mucopurulent discharge. A chronic unilateral purulent nasal discharge lasting several weeks or months in horses suggests nasal granulomas associated with mycotic infections.4,5
‘Summer snuffles’ of cattle presents a characteristic syndrome involving several animals in a herd. Cases occur in the spring and autumn when the pasture is in flower and warm moist environmental conditions prevail. The disease may be most common in Channel Island breeds. There is a sudden onset of dyspnea with a profuse nasal discharge of thick, orange to yellow material that varies from a mucopurulent to caseous consistency. Sneezing, irritation, and obstruction are severe. The irritation may cause the animal to shake its head, rub its nose along the ground or poke its muzzle repeatedly into hedges and bushes. Sticks and twigs may be pushed up into the nostrils as a result and cause laceration and bleeding. Stertorous, difficult respiration accompanied by mouth breathing may be evident when both nostrils are obstructed. In the most severe cases a distinct pseudomembrane is formed that is later snorted out as a complete nasal cast. In the chronic stages multiple proliferative non-erosive nodules 2–8 mm in diameter and 4 mm high with marked mucosal edema are visible in the anterior nares.7
In familial allergic rhinitis in cattle, the clinical signs begin in the spring and last until late fall.2 Affected animals exhibit episodes of violent sneezing and extreme pruritus manifested by rubbing their nostrils on the ground, trees, and other inanimate objects and frequently scratching the nares with their hind feet. Dyspnea and loud snoring sounds are common and affected animals frequently clean their nostrils with their tongues. The external nares contain a thick mucoid discharge and the nasal mucosa is edematous and hyperemic. The clinical abnormalities resolve during the winter months. All affected animals are positive to intradermal skin testing for a wide variety of allergens.
Mycotic rhinitis in the horse is characterized by noisy respirations, circumferential narrowing of both nasal passages and thickening of the nasal septum. The nasal conchae and turbinates may be roughened and edematous, and the ventral meati decreased in size bilaterally. The nasal discharge may be unilateral or bilateral. Endoscopically, granulomas may be found in almost any location in the nasal cavities and extending on to the soft palate and into the maxillary sinus.5 The disease is discussed in detail in Chapter 24.
Endoscopic examination using a flexible fiberoptic endoscope or a rigid endoscope is very useful for the visual inspection of lesions affecting the nasal mucosae of horses and cattle that are not visible externally. Radiographic or computed tomographic imaging can be used to detect atrophic rhinitis, although use of these techniques on a wide scale is clearly not practical.8
Examination of nasal swabs of scrapings for bacteria, inclusion bodies or fungi may aid in diagnosis. Discharges in allergic rhinitis usually contain many more eosinophils than normal. Nasal mucosal biopsy specimens are useful for microbiological and histopathological examination.3
Rhinitis is not a fatal condition, although animals may die of specific diseases in which rhinitis is a prominent lesion.
Rhinitis is readily recognizable clinically. Differentiation of the specific diseases listed under Etiology, above, is discussed under their respective headings.
Allergic rhinitis in cattle must be differentiated from maduromycosis, rhinosporidiosis, and infection with the pasture mite (Tyrophagus palmarum). The differential diagnosis may be difficult if allergic rhinitis occurs secondary to some of these infections.
Rhinitis in the horse must be differentiated from inflammation of the facial sinuses or guttural pouches in which the nasal discharge is usually purulent and persistent and often unilateral, and there is an absence of signs of nasal irritation. A malodorous nasal discharge, frontal bone distortion, draining tracts at the poll, and neurological abnormalities are common in cattle with chronic frontal sinusitis as a complication of dehorning.9
Specific treatment aimed at control of individual causative agents is described under each disease. Thick tenacious exudate that is causing nasal obstruction may be removed gently and the nasal cavities irrigated with saline. A nasal decongestant sprayed up into the nostrils may provide some relief. Newborn piglets with inclusion body rhinitis may be affected with severe inspiratory dyspnea and mouth-breathing that interferes with sucking. The removal of the exudate from each nostril followed by irrigation with a mixture of saline and antimicrobials will provide relief and minimize the development of a secondary bacterial rhinitis. Animals affected with allergic rhinitis should be taken off the pasture for about a week and treated with antihistamine preparations.
Nasal obstruction occurs commonly in cattle and sheep. The disease is usually chronic and due to:
• In sheep, infestation with Oestrus ovis
• In cattle, most often enzootic nasal granuloma, acute obstruction or the allergic condition ‘summer snuffles’. Cystic enlargement of the ventral nasal conchae in cattle can cause unilateral10 or bilateral nasal obstruction.11
Minor occurrences include the following:
• Large mucus-filled polyps developing in the posterior nares of cattle and sheep and causing unilateral or bilateral obstruction
• Granulomatous lesions caused by a fungus, Rhinosporidium sp. and by the blood fluke, Schistosoma nasalis
• A chronic pyogranuloma due to Coccidioides immitis infection has occurred in the horse12
• Foreign bodies may enter the cavities when cattle rub their muzzles in bushes in an attempt to relieve the irritation of acute allergic rhinitis
• Nasal amyloidosis occurs rarely in mature horses and is characterized clinically by stertorous breathing and raised, firm, nonpainful, nodular swellings on the rostral nasal septum and floor of the nasal cavity.13 Affected horses do not have any other illness and surgical removal of the lesions is recommended
• Infestation of the nasopharynx of horses by Gasterophilus pecorum causes obstruction of the upper airway.14
Neoplasms of the olfactory mucosa are not common but do occur, particularly in sheep, goats, and cattle, where the incidence in individual flocks and herds may be sufficiently high to suggest an infectious cause.15 The lesions are usually situated just in front of the ethmoid bone, are usually unilateral but may be bilateral and have the appearance of adenocarcinomas of moderate malignancy. In cattle, the disease is commonest in 6–9-year-olds and may be sufficiently extensive to cause bulging of the facial bones. The tumors are adenocarcinomas arising from the ethmoidal mucosa, and they metastasize in lungs and lymph nodes. Clinical signs include nasal discharge, often bloody, mouth-breathing and assumption of a stretched-neck posture. There is evidence to suggest that a virus may be associated. A similar syndrome is observed in cattle with other nasal tumors such as osteoma.
Neoplasia that obstructs the nasal cavity occurs in horses with squamous cell carcinoma or adenocarcinoma of the sinus or nasal cavity, angiosarcoma and a variety of other rare tumors.16 Epidermal inclusions cysts of the nasal diverticulum of horses can cause obstruction of the nasal cavity, but are not neoplasms.17 Cysts of the paranasal sinuses can cause marked facial deformity and obstruction to air passages.18
Enzootic nasal adenocarcinoma occurs in sheep and goats.15 The disease is sporadic but has occurred in related flocks, which suggests that it may be an enzootic problem. The clinical findings include a persistent serous, mucous, or mucopurulent nasal discharge and stridor. Affected sheep progressively develop anorexia, dyspnea, and mouth-breathing and most die within 90 days after the onset of signs. The tumors originate unilaterally or occasionally bilaterally in the olfactory mucosa of the ethmoid turbinates. They are locally invasive but not metastatic. Histologically the tumors are classified as adenomas or, more frequently, adenocarcinomas. The etiology is unknown, but a retrovirus may be involved. Budding and extracellular retrovirus-like particles have been observed ultrastructurally in enzootic nasal tumors of goats.15
Ethmoidal hematomas are encapsulated, usually expanding, insidious, potentially distorting and obstructing lesions of the nasal cavities that occur in horses.19 Chronic unilateral nasal discharge is common and lesions are usually advanced at the time of diagnosis. There is stertorous breathing and upper airway obstruction in later stages of the disease. The nasal discharge is serous or mucoid and intermittently sanguineous, sanguinopurulent and usually unrelated to exercise. Diagnosis is made by endoscopy and radiography. Surgical removal is possible and successful in some cases. Multiple intralesional injection of formalin (1–100 mL of 10% neutral buffered formalin injected at 10 day intervals) through an endoscope can cure the tumor but there is the risk of serious adverse effects if the ethmoidal hematoma penetrates the cribriform plate.5,20 The procedure involves the injection of a sufficient volume of 10% neutral buffered formalin to distend the lesion. The formalin is injected via an endoscope once every 10 days until the lesion resolves by sloughing. Between one and 20 injections are required. However, the prognosis for long-term resolution of the tumor is poor because of high rates of recurrence.
In cattle, sheep, and pigs there is severe inspiratory dyspnea when both cavities are blocked. The animals may show great distress and anxiety and breathe in gasps through the mouth. Obstruction is usually not complete and a loud, wheezing sound occurs with each inspiration. A nasal discharge is usually present but varies from a small amount of blood-stained serous discharge when there is a foreign body present to large quantities of purulent exudate in allergic rhinitis. Shaking of the head and snorting are also common signs. If the obstruction is unilateral the distress is not so marked and the difference in breath streams between the two nostrils can be detected by holding the hands in front of the nose. The magnitude of the air currents from each nostril on expiration can be assessed with the aid of a piece of cotton thread (watching the degree of deflection). The passage of a stomach tube through each nasal cavity may reveal evidence of a space-occupying lesion. The diameter of the tube to be used should be one size smaller than would normally be used on that animal to insure that the tube passes easily. The signs may be intermittent when the obstruction is caused by a pedunculated polyp in the posterior nares.
Treatment must be directed at the primary cause of the obstruction. Removal of foreign bodies can usually be effected with the aid of long forceps, although strong traction is often necessary when the obstructions have been in position for a few days. As an empirical treatment in cattle oral or parenteral administration of iodine preparations is in general use in chronic nasal obstruction.
1 Wiseman A, et al. Vet Rec. 1982;110:420.
2 Krahwinkel DJ, et al. J Am Vet Med Assoc. 1988;192:1593.
3 Shibahara T, et al. Aust Vet J. 2001;79:363.
4 Davis PR, et al. J Am Vet Med Assoc. 2000;217:707.
5 Marriott MR, et al. Aust Vet J. 1999;77:371.
6 Watson PJ, et al. Vet Rec. 2003;153:704.
7 Olchowy TWJ, et al. J Am Vet Med Assoc. 1995;207:1211.
8 Frame EM, et al. Vet Rec. 2000;146:558.
9 Ward JL, Rebhun WC. J Am Vet Med Assoc. 1992;201:326.
10 Jean GS, Robertson JT. Aust Vet J. 1987;28:251.
11 Ross MW, et al. J Am Vet Med Assoc. 1986;188:857.
12 Hodgin EC, et al. J Am Vet Med Assoc. 1984;184:339.
13 Shaw J, Sautet JY. Vet Pathol. 1987;24:183.
14 Smith MA, et al. Vet Rec. 2005;156:283.
15 De Las Heras M, et al. Vet Pathol. 1991;28:474.
16 Dixon PM, Head KW. Vet J. 1999;157:279.
17 Frankeny RL. J Am Vet Med Assoc. 2003;223:221.
18 Lane J, et al. Equine Vet J. 1987;19:537.
19 Stich KL, et al. Compend Contin Educ Pract Vet. 2001;23:1094.
Epistaxis is bleeding from the nostrils regardless of the origin of the hemorrhage, and hemoptysis is the coughing up of blood, with the hemorrhage usually originating in the lungs. Both epistaxis and hemoptysis are important clinical signs in cattle and horses. The bleeding may be in the form of a small volume of blood-stained serous discharge coming from the nose only, or it can be a large volume of whole blood coming precipitously from both nostrils and sometimes the mouth. The first and most important decision is to determine the exact location of the bleeding point.
Epistaxis occurs commonly in the horse and may be due to lesions in the nasal cavity, nasopharynx, auditory tube diverticulum (guttural pouch) or lungs (see Table 10.5). Exercise-induced pulmonary hemorrhage is described under that heading earlier in this chapter.
Hemorrhagic lesions of the nasal cavity, nasopharynx, and guttural pouch in the horse usually cause unilateral epistaxis of varying degree depending on the severity of the lesions. Pulmonary lesions in the horse resulting in hemorrhage into the lumen of the bronchi also result in epistaxis. Blood originating from the lungs of the horse is discharged most commonly from the nostrils and not the mouth because of the horse’s long soft palate. Also, blood from the lungs of the horse is not foamy when seen at the nose because the horizontal position of the major bronchi allows blood to flow out freely without being coughed up and made foamy. It was previously thought that upper respiratory tract hemorrhage could be distinguished from lower respiratory tract hemorrhage by the blood in the latter case being foamy. This does not apply in the horse. Froth is usually the result of pulmonary edema, in which case it is a very fine, pink, stable froth.
Bleeding from lesions of the upper respiratory tract of horses usually occur spontaneously while the horse is at rest. One of the commonest causes of unilateral epistaxis in the horse is mycotic ulceration of the blood vessels in the wall of the guttural pouch (guttural pouch mycosis).
Other less common causes of nasal bleeding include hemorrhagic polyps of the mucosa of the nasal cavity or paranasal sinuses, and encapsulated hematomas, which look like hemorrhagic polyps, commencing near the ethmoidal labyrinth and expanding into the nasal cavity and the pharynx. There is respiratory obstruction, coughing, choking, and persistent unilateral epistaxis. The capsule of the hematoma is respiratory epithelium. Surgical correction has been achieved. Another cause, most uncommonly, is a parasitic arteritis of the internal carotid artery as it courses around the guttural pouch.1
Mild epistaxis is a common finding in horses and cattle with severe thrombocytopenia.2
Erosions of the nasal mucosa in glanders, granulomatous and neoplastic diseases and trauma due to passage of a nasal tube or endoscope, or from physical trauma externally, are other obvious causes.
A case of fibrous dysplasia in the ventral meatus of a horse with epistaxis is recorded.3 Similarly, in congestive heart failure and purpura hemorrhagica there may be a mild epistaxis.
Neoplasia, and notably hemangiosarcoma, of the upper or lower respiratory tract can cause epistaxis.4
Envenomation of horses by rattlesnakes in the western USA caused a clinical syndrome that includes swelling of the head, dyspnea, and epistaxis.5
Poisoning by bracken fern or moldy sweet clover is a common cause of spontaneous epistaxis in cattle. The epistaxis may be bilateral, and hemorrhages of other visible and subcutaneous mucous membranes are common. An enzootic ethmoidal tumor has been described in cattle in Brazil and was at one time a disease of some importance in Sweden.6 The lesion occupies the nasal cavities, causes epistaxis and may invade paranasal sinuses.
In hemoptysis in horses the blood flows along the horizontal trachea and pools in the larynx until the swallowing reflex is stimulated and swallowing occurs; or coughing is stimulated and blood is expelled through the mouth and nostrils. In some horses repeated swallowing, without eating or drinking, can be a good indicator that bleeding is occurring. The origin of the hemorrhage is usually in the lungs and in cattle the usual cause is a pulmonary arterial aneurysm and thromboembolism from a posterior vena caval thrombosis, usually originating from a hepatic abscess.7 Recurrent attacks of hemoptysis with anemia and abnormal lung sounds usually culminate in an acute intrapulmonary hemorrhage and rapid death.
The origin of the hemorrhage in epistaxis and hemoptysis may be obvious, as in traumatic injury to the turbinates during passage of a stomach tube intranasally or if a systemic disease with bleeding defects is present. In many other cases, however, the origin of the hemorrhage is not obvious and special examination procedures may be required. Careful auscultation of the lungs for evidence of abnormal lung sounds associated with pulmonary diseases is necessary.
The nasal cavities should be examined visually with the aid of a strong, pointed source of light through the external nares. Only the first part of the nasal cavities can be examined directly but an assessment of the integrity of the nasal mucosa can usually be made. In epistaxis due to systemic disease or clotting defects the blood on the nasal mucosa will usually not be clotted. When there has been recent traumatic injury to the nasal mucosa or erosion of a blood vessel by a space-occupying lesion such as tumor or nasal polyp, the blood will usually be found in clots in the external nares.
The nasal cavities should then be examined for any evidence of obstruction as set out in the previous section. When the blood originates from a pharyngeal lesion there are frequent swallowing movements and a short explosive cough, which may be accompanied by the expulsion of blood from the mouth. Hematological examinations are indicated to assist in the diagnosis of systemic disease or clotting defects. Radiological examinations of the head are indicated when space-occupying lesions are suspected.
In the horse, the use of the flexible fiberoptic endoscope will permit a thorough examination of the nasal cavities, nasopharynx, guttural pouch and larynx, trachea and major bronchi.
Specific treatment of epistaxis and hemoptysis depends on the cause. Hemorrhage from traumatic injuries to the nasal mucosa does not usually require any treatment. Space-occupying lesions of the nasal mucosa may warrant surgical therapy. Epistaxis associated with guttural pouch mycosis may require ligation of the affected artery. The ineffectiveness of therapy for exercise-induced pulmonary hemorrhage has been discussed above. There is no successful treatment for the hemoptysis due to pulmonary aneurysm and posterior vena caval thrombosis in cattle. General supportive therapy is as for any spontaneous hemorrhage and includes rest, blood transfusions, and hematinics.
1 Owen RR. Equine Vet J. 1974;6:143.
2 Hoyt PG, et al. J Am Vet Med Assoc. 2000;217:717.
3 Livesey MA, et al. Equine Vet J. 1984;16:144.
4 Southwood LL, et al. J Vet Intern Med. 2000;14:105.
5 Dickinson C.E., et al. J Am Vet Med Assoc. 1996;208:1866.
Inflammation of the air passages usually involves all levels and no attempt is made here to differentiate between inflammations of various parts of the tract. They are all characterized by cough, noisy inspiration and some degree of inspiratory embarrassment.
All infections of the upper respiratory tract cause inflammation, either acutely or as chronic diseases. In most diseases the laryngitis, tracheitis, and bronchitis form only a part of the syndrome and the causes listed below are those diseases in which upper respiratory infection is a prominent feature.
• Infectious bovine rhinotracheitis (bovine herpesvirus-1), calf diphtheria (necrotic laryngitis), Histophilus somnus
• Tracheal stenosis in feedlot cattle, ‘honker cattle’, etiology unknown1
• Congenital cavitation of the arytenoid may contribute to laryngeal abscess development
• Syngamus laryngeus infests the larynx of cattle in the tropics.
• Equine herpesvirus (EVR), equine viral arteritis (EVA), equine viral influenza (EVI), strangles (S. equi)
• Idiopathic ulceration of the mucosa covering the arytenoid cartilages.2
Irritation of the mucosa causes frequent coughing, and swelling causes partial obstruction of the air passages, with resulting inspiratory dyspnea. Necrotic laryngitis in calves is associated with marked changes in pulmonary function, modifies tracheal dynamics and disturbs the growth process by increasing the energetic cost of breathing; this can result in impaired feed intake and predisposition to secondary pulmonary infection and subsequent respiratory failure from progressive exhaustion.3
Coughing and inspiratory dyspnea with laryngeal roaring or stridor are the common clinical signs. In the early stages of acute infections the cough is usually dry and nonproductive and is easily induced by grasping the trachea or larynx, or by exposure to cold air or dusty atmospheres. In acute laryngitis, the soft tissues around the larynx are usually enlarged and painful on palpation. In chronic affections, the cough may be less frequent and distressing and is usually dry and harsh. If the lesions cause much exudation or ulceration of the mucosa, as in bacterial tracheobronchitis secondary to infectious bovine rhinotracheitis in cattle, the cough is moist, and thick mucus, flecks of blood and fibrin may be coughed up. The cough is very painful and the animal makes attempts to suppress it. Fever and toxemia are common and affected animals cannot eat or drink normally.
Inspiratory dyspnea varies with the degree of obstruction and is usually accompanied by a loud stridor and harsh breath sounds on each inspiration. These are best heard over the trachea although they are quite audible over the base of the lung, being most distinct on inspiration. The respiratory movements are usually deeper than normal and the inspiratory phase more prolonged and forceful. Additional signs, indicative of the presence of a primary specific disease, may also be present.
Examination of the larynx is usually possible through the oral cavity using a cylindrical speculum of appropriate size and a bright, pointed source of light. This is done relatively easily in cattle, sheep, and pigs but is difficult in the horse. Lesions of the mucosae of the arytenoid cartilages and the vault of the larynx are usually visible if care and time are taken. In laryngitis, there is usually an excessive quantity of mucus, which may contain flecks of blood or pus in the pharynx. Palpation of the pharyngeal and laryngeal areas may reveal lesions not readily visible through a speculum. During opening of the larynx, lesions in the upper part of the trachea are sometimes visible. The use of a fiberoptic endoscope allows a detailed examination of the upper respiratory tract.
Inflammation or lesions of the larynx may be severe enough to cause marked inspiratory dyspnea and death from asphyxia. In calves and young cattle with diphtheria the lesion may be large enough (or have a pedicle and act like a valve) to cause severe inspiratory dyspnea, cyanosis, anxiety and rapid death. The excitement associated with loading for transportation to a clinic or of a clinical examination, particularly the oral examination of the larynx, can exaggerate the dyspnea and necessitate an emergency tracheotomy.
Most cases of bacterial laryngitis will heal without obvious residual sign after several days of antimicrobial therapy. Some cases in cattle become chronic in spite of therapy due to the inflammation extending down into the arytenoid cartilages resulting in a chronic chondritis due to a sequestrum similar to osteomyelitis. Abscess formation is another common cause of chronicity. Secondary bacterial infection of primary viral diseases, or extension of bacterial infections to the lungs commonly results in pneumonia.
Tracheal stenosis in cattle is characterized by extensive edema and hemorrhage of the dorsal wall of the trachea, resulting in coughing (honking), dyspnea and respiratory stertor.1 Complete occlusion of the trachea may occur. Affected animals may be found dead without any premonitory signs.
Laboratory examinations may be of value in determining the presence of specific diseases.
Upper respiratory infections are not usually fatal but lesions vary from acute catarrhal inflammation to chronic granulomatous lesions depending upon the duration and severity of the infection. When secondary bacterial invasion occurs a diphtheritic pseudomembrane may be present and be accompanied by an accumulation of exudate and necrotic material at the tracheal bifurcation and in the dependent bronchi.
Inflammation of the larynx usually results in coughing, and inspiratory dyspnea with a stertor and loud abnormal laryngeal sounds on auscultation over the trachea and over the base of the lungs on inspiration. Lesions of the larynx are usually visible by laryngoscopic examination, those of the trachea and major bronchi are not so obvious unless special endoscopic procedures are used. Every reasonable effort should be used to inspect the larynx and trachea. Obstruction of the nasal cavities and other parts of the upper respiratory tract may also be difficult to distinguish unless other signs are present.
Most of the common viral infections of larynx, trachea, and major bronchi will resolve spontaneously if the affected animals are rested, not worked and not exposed to inclement weather and dusty feeds. Secondary bacterial complications must be recognized and treated with the appropriate antimicrobial.
The bacterial infections can result in severe inflammation with necrosis and granulomatous lesions and must be treated with antimicrobials. Calves with calf diphtheria should be treated with a broad-spectrum antimicrobial daily for 3–5 days. Several days are usually required for the animal to return to normal. A broad-spectrum antimicrobial daily or more often for up to 3 weeks or more may be necessary for treatment of the chondritis.
NSAIDs such as flunixin meglumide may be used in an attempt to reduce the laryngeal edema associated with some severe cases of bacterial laryngitis in cattle.
Animals with severe lesions and marked inspiratory dyspnea may require a tracheotomy and insertion of a tracheotomy tube for several days until the lesion heals. The tube must be removed, cleaned out and replaced at least once daily because of the accumulation of dried mucus plugs which interfere with respiration. The techniques of tracheotomy and permanent tracheostomy in the horse have been described.4,5 Surgical excision of chronic granulomatous lesions and abscesses of the larynx may be indicated following failure of long-term antimicrobial therapy but postoperative complications of laryngeal and pharyngeal paralysis may occur. Laryngotomy as a treatment for chronic laryngeal obstruction in cattle with long-term survival of 58% has been described.6
Tracheolaryngostomy of calves with chronic laryngeal obstruction due to necrobacillosis has been used with a high degree of success.7 Under general anesthesia and dorsal recumbency, an incision is made over the lower third of the thyroid and cricoid cartilages and the first two tracheal rings.7 The larynx is easily visualized and necrotic tissue removed using a curette. The edges of the cartilages are sutured closed. A wedge-shaped piece of the first two tracheal rings is removed to create a tracheostomy, which is allowed to close after about 1 week when the postoperative swelling has subsided with the aid of daily care of the surgical site and the possible use of flunixin meglumide.7 No tracheotomy tube is required.
Traumatic laryngotracheal injury can occur following endotracheal intubation used for general anesthesia.1 Nasotracheal intubation can result in mucosal injury to the nasal meatus, the arytenoid cartilages, the trachea, the dorsal pharyngeal recess, the vocal cords and the entrance to the guttural pouches.1 The laryngeal injury is attributed to the tube pressure on the arytenoid cartilages and vocal folds and the tracheal damage is due to the pressure exerted by the inflated cuff on the tracheal mucosa.
Tracheal collapse occurs in calves,2,3 in mature cattle,4 in goats and in horses, including miniature horses and foals.5 Dynamic collapse is a cause of exercise intolerance in race horses that is evident only by endoscopic examination of the trachea during strenuous exercise.6 Restriction of the tracheal lumen and laxity of the dorsal tracheal membrane results in varying degrees of inspiratory dyspnea with stridor, coughing, and reduced exercise tolerance. A ‘honking’ respiratory noise is common in affected calves when coughing spontaneously or when the trachea is palpated. Tracheal collapse in calves is associated with injuries associated with dystocia and clinical signs usually occur within a few weeks after birth. In some cases the trachea is compressed at the level of the thoracic inlet in association with callus formation of healing fractured ribs attributed to dystocia. In some cases in cattle, there is no history of dystocia or pre-existing disease or previous manipulation of the trachea and the overall lumen size may be reduced to less than 25% of normal.7 Auscultation of the thorax may reveal loud referred upper airway sounds. Tracheal prostheses have been used for the treatment of tracheal collapse in calves and Miniature horses.8
Tracheal obstruction and collapse can result from tracheitis associated with pneumonia in the horse, tracheal neoplasia, tracheal stricture, presence of foreign bodies in the trachea and compression by masses external to the trachea.5,9 It is suggested that increased respiratory effort associated with pneumonia causes collapse of the soft tissue structures of the trachea, rather than collapse of the tracheal rings. Tracheal rupture due to blunt trauma in the horse may result in severe subcutaneous emphysema and pneumomediastinum.4 Conservative therapy is usually successful. Tracheal compression secondary to enlargement of the cranial mediastinal lymph nodes can also cause inspiratory dyspnea10 and conservative treatment with antimicrobials is successful.
1 Holland M, et al. J Am Vet Med Assoc. 1986;189:1447.
2 Jelinski M, Vanderkop M. Aust Vet J. 1990;31:783.
3 Fingland RB, et al. Vet Surg. 1990;19:371.
4 Fubini SL, et al. J Am Vet Med Assoc. 1985;187:69.
5 Fenger CK, Kohn CW. J Am Vet Med Assoc. 1992;200:1698.
6 Tetens J, et al. J Am Vet Med Assoc. 2000;216:722.
7 Ashworth CD, et al. Can Vet J. 1992;33:50.
8 Couetil LL, et al. J Am Vet Med Assoc. 2004;225:1727.
Pharyngitis in all species is associated with infectious diseases of the upper airway. It is most studied in horses, probably because of the frequency of examination of the upper airway in this species. Pharyngitis in horses has many similarities to tonsillitis in children.1 The disorder in horses involves follicular lymphoid hyperplasia of the pharynx and involves both the pharyngeal tonsil and the extensive and diffuse lymphoid tissue in the walls and dorsal aspect of the pharynx. These tissues form the mucosal associated lymphoid tissues and are an important component of the normal immunological response of horses.2 The condition occurs in approximately 34% of Thoroughbred race horses3 and is probably as common in other breeds of horse. The condition is first detectable in 2–3-month-old foals and reaches its highest prevalence and greatest severity in yearlings and 2-year-old horses in race training.4 It is evident on endoscopic examination as diffuse, multiple, small, white nodules in the roof and walls of the pharynx. The nodules can be confluent and there is often excessive mucus present in severely affected horses. The clinical significance of the condition is debated. Affected race horses do not have impaired race performance.4 Affected horses recover spontaneously as they age, or after treatment with topical anti-inflammatory drugs. The condition is probably a normal aging process and necessary for development of a competent immune system in young horses.1
Infestation of the nasopharynx of horses by larvae of the bot fly Gasterophilus pecorum causes obstruction of the upper airway and a parasitic pharyngitis.5 Diagnosis is by visualization of the parasite during endoscopic examination.
Obstruction of the upper airway is a common cause of exercise intolerance in horses and is characterized in most cases by unusual respiratory noise during heavy exercise.
The cause of laryngeal hemiplegia is degeneration of the recurrent laryngeal nerve with subsequent neurogenic atrophy of the cricoarytenoid dorsalis and other intrinsic muscles of the larynx.1 The etiology of neuronal degeneration is unknown but the pathological changes are typical of a distal axonopathy.1 The disease is usually idiopathic but occasional cases are caused by guttural pouch mycosis or inadvertent perivascular injection of irritant material, such as phenylbutazone, around the jugular vein and vagosympathetic trunk. Bilateral laryngeal paralysis is usually associated with intoxication (organophosphate, haloxon) or trauma from endotracheal intubation during general anesthesia.
The disease affects large horses more commonly than ponies, and it is commonly recognized in draft horses, Thoroughbreds, Standardbreds, Warmbloods and other breeds of large horse. The prevalence of laryngeal hemiplegia in Thoroughbred horses in training is between 1.8 and 13%2-4 depending, among other factors, on the criteria used to diagnose the condition. Among apparently normal Thoroughbred horses examined after racing, grade 4 laryngeal hemiplegia was detected in 0.3% of 744 horses, grade 3 in 0.1%, and grade 2 in 1.1%.5 Male horses over 160 cm tall are at most risk of developing the disease.6 There is evidence of a familial distribution of the disease with offspring of affected parents being more frequently affected (61%) than adult offspring of unaffected parents (40%).7
Axonal degeneration causes preferential atrophy of the adductor muscles of the larynx, although both adductor (dorsal cricoarytenoid muscle) and adductor (lateral cricoarytenoid muscle) are involved.8 Fiber-type grouping of laryngeal muscles, evidence of recurrent laryngeal neuropathy, is present in draft foals as young as 2 weeks of age, indicating an early onset of the disease.9 The disease is progressive in some horses.10
Compromised function of the adductor muscles results in partial occlusion of the larynx by the arytenoid cartilage and vocal fold during inspiration. The obstruction is most severe when airflow rates through the larynx are large, such as during strenuous exercise. Laryngeal obstruction increases the work of breathing, decreases the maximal rate of oxygen consumption and exacerbates the hypoxemia and hypercarbia normally associated with strenuous exercise by horses.11,12 These effects result in a severe limitation to athletic capacity and performance.
Clinical findings include exercise intolerance and production of a whistling or roaring noise during strenuous exercise. The disease can be detected by analysis of respiratory noise.13
Endoscopic examination of the upper airway provides the definitive diagnosis in most cases. Examination of the larynx is performed with the horse at rest and the position and movement of the arytenoid cartilages assessed. Laryngeal function can also be observed during swallowing, brief (30–60 s) bilateral nasal occlusion, and during and after exercise. Endoscopic examination during strenuous exercise on a treadmill of horses with grade III disease may be beneficial in determining the severity of the disease.14,15 Horses with early or mild degeneration of the recurrent laryngeal nerve and associated laryngeal musculature can have normal laryngeal function at rest. However, the loss of muscle function becomes apparent during exercise, when the laryngeal muscles of affected animals fatigue more rapidly than do those of normal animals, with the result that laryngeal dysfunction can become apparent during or immediately after exercise. Endoscopic examination during exercise is useful in differentiating the disease from axial deviation of the aryepiglottic folds.16
The severity of the disease is graded I through IV:
• Grade I is normal, there being synchronous, full abduction and adduction of both arytenoid cartilages
• Grade II presents as weakness of the adductors evident as asynchronous movement and fluttering of the arytenoid cartilage during inspiration and expiration, but with full abduction during swallowing or nasal occlusion
• Grade III has asynchronous movement of the arytenoid cartilage during inspiration or expiration; full abduction is not achieved during swallowing or nasal occlusion
• Grade IV implies marked asymmetry of the larynx at rest and no substantial movement of the arytenoid cartilage during respiration swallowing or nasal occlusion.17
There are no characteristic changes in the hemogram or in serum biochemical variables in resting horses. During exercise there is a marked exacerbation of the normal exercise-induced hypoxemia and the development of hypercapnia in affected horses.11,12
Lesions are confined to an axonopathy of the recurrent laryngeal nerves and neurogenic muscle atrophy of the intrinsic muscles of the larynx.
Diagnostic confirmation is achieved by endoscopic examination of the larynx.
Differential diagnoses of exercise intolerance and exercise-induced respiratory noise include:
• Dorsal displacement of the soft palate
• Aryepiglottic fold entrapment
• Axial deviation of the aryepiglottic folds16
1 Cahill JI, Goulden BE. N Z Vet J. 1986;34:161.
2 Lane JG, et al. Equine Vet J. 1987;19:531.
3 Sweeney CR, et al. J Am Vet Med Assoc. 1991;198:1037.
4 Hillidge CJ. Vet Rec. 1986;118:535.
5 Brown JA, et al. Equine Vet J. 2005;37:397.
6 Cahill JI. Goulden N Z Vet J. 1987;35:82.
7 Ohnesorge B, et al. Zentralbl Vet A. 1993;40:134.
8 Duncan ID, et al. Equine Vet J. 1991;23:94.
9 Harrison GD, et al. Acta Neuropathol. 1992;84:307.
10 Dixon PM, et al. Equine Vet J. 2002;34:29.
11 Christley RM, et al. Equine Vet J. 1997;29:6.
12 King CM, et al. Equine Vet J. 1994;26:220.
13 Cable CS, et al. Am J Vet Res. 2002;63:1707.
14 Hammer EJ, et al. J Am Vet Med Assoc. 1998;212:399.
15 Dart AJ, et al. Aust Vet J. 2001;79:109.
The soft palate of equids is unique in that it provides an airtight seal between the oropharynx and nasopharynx during respiration. The horse is an obligate nasal breather except during very unusual circumstances. During swallowing the soft palate is transiently displaced dorsally as part of the normal act of deglutition to permit passage of the feed bolus. Displacement of the soft palate other than during deglutition is abnormal and can be intermittent, which is usually associated with exercise, or persistent, which is usually associated with disruption of the nerve supply to the pharynx.
Intermittent dorsal displacement of the soft palate occurs during exercise in some horses and causes an expiratory obstruction to air flow through the larynx and pharynx. Estimates of the prevalence of the disease are unreliable because of the transient nature of the displacement and the fact that it only occurs during exercise. It is estimated to occur in 0.5–1.3% of Thoroughbred race horses.1 The cause of intermittent displacement of the soft palate during exercise is unknown, although a number of mechanisms, including palatal myositis,2 ulcers of the caudal border of the soft palate, caudal retraction of the larynx and lower respiratory disease, are suggested. Retropharyngeal lymphadenopathy can cause neurogenic paresis of the pharyngeal and palatal muscles, with dorsal displacement of the soft palate the most obvious sign of pharyngeal collapse during exercise.3 The immediate cause of the displacement is the negative intrapharyngeal pressure generated during exercise.
Displacement of the soft palate during strenuous exercise places the soft palate dorsal to the epiglottis, a position in which it impedes flow of air during expiration.4 Peak expiratory airflow, minute ventilation, tidal volume and rate of oxygen consumption are all decreased in horses with dorsal displacement of the soft palate, whereas inspiratory flow and breathing rate are not affected.4
The clinical signs include exercise intolerance and intermittent production of a gurgling noise during strenuous exercise. Endoscopic examination of resting horses usually demonstrates a normal pharynx and larynx. Brief nasal occlusion (30–60 s) that induces displacement of the soft palate, in combination with a history of respiratory noise during exercise, increases the likelihood of the disorder. Endoscopic examination of affected horses during or immediately after exercise may reveal dorsal displacement of the soft palate. Radiographic examination of the pharynx may reveal a shortened epiglottis (< 7 cm) in some affected horses.
Differential diagnoses for exercise intolerance and respiratory noise include laryngeal hemiplegia, subepiglottic cysts, arytenoid chondritis and aryepiglottic fold entrapment. The important differentiating factor is that the noise occurs predominantly during expiration, and has a more gurgling sound to it than does the noise produced by horses with laryngeal hemiplegia.
There is no definitive treatment. Usual methods of surgical intervention include augmentation of the epiglottis by injection of polytetrafluoroethylene (Teflon) paste, resection of the caudal edge of the soft palate or sternothyrohyoideus myectomy,5 although some of these interventions may have deleterious effects on upper airway airflow.6 A newer surgical technique involves the ‘laryngeal tie-forward’ procedure.7 Reports of success of surgical treatment of the disease are not definitive, in part because horses with the disorder that went untreated are not examined. It is plausible that the response to surgical treatment could be the result of enforced rest rather than the manipulation. Treatment of retropharyngeal lymphadenopathy may be beneficial. Nonsurgical treatment includes the use of anti-inflammatory drugs, tongue-ties, a variety of bits and a laryngohyoid support apparatus.8
Persistent dorsal displacement of the soft palate is usually the result of damage to the innervation of the pharyngeal and palatal muscles as a result of:
• Retropharyngeal lymph node abscessation
• Equine protozoal myeloencephalitis
Blockade of the pharyngeal branch of the vagus nerve by injection of local anesthetic causes persistent dorsal displacement of the soft palate whereas blockade of the hypoglossal and glossopharyngeal nerves does not.9,10
Persistent dorsal displacement of the soft palate causes dysphagia and stertorous respiration. Food material discharges from the nares and there is frequent coughing, probably secondary to the aspiration of feed material. Affected horses may develop aspiration pneumonia. If the condition persists, there is dehydration and weight loss. Endoscopic examination of the upper airways reveals dorsal displacement of the soft palate and may reveal other abnormalities, such as guttural pouch mycosis, that may provide a cause for the disease.
1 Brown JA, et al. Equine Vet J. 2005;37:397.
2 Blythe LL, et al. J Am Vet Med Assoc. 1983;183:781.
3 Derksen FJ, et al. In: Proceedings of the Dubai International Equine Symposium 1997:23.
4 Franklin SH, et al. Equine Vet J Suppl. 2002;34:379.
5 Smith JJ, Emberstson RM. Vet Surg. 2005;34:5.
6 Holcombe SJ, et al. J Appl Physiol. 1994;77:2812.
7 Woodie JB, et al. Equine Vet J. 2005;37:418.
8 Woodie JB, et al. Equine Vet J. 2005;37:425.
Entrapment of the epiglottis in the fold of tissue that extends from the arytenoid cartilage to the ventrolateral aspect of the epiglottis causes exercise intolerance and respiratory noise during exercise in racehorses.1 The disorder occurs in both young and mature race horses, and is found in approximately 1% of Thoroughbred race horses.2,3 The entrapment is often detected during rhinolaryngoscopic examination of racehorses, although it might not be the cause of poor performance.3 The presence of aryepiglottic fold entrapment causes a predominantly expiratory obstruction to air flow across the larynx during exercise. The interference with airflow, if any, does not appreciably impair performance in all horses.3
Clinical signs are of exercise intolerance and respiratory noise during exercise. Acute cases can be associated with epiglottitis, whereas chronic cases are usually an incidental finding during endoscopic examination of the upper airway.
Endoscopic examination of the upper airway reveals the border of the epiglottis to be obscured by the aryepiglottic folds. Normally, the serrated margin of the epiglottis and dorsal blood vessels extending to the lateral margins of the epiglottis are readily apparent, but when the epiglottis is entrapped these features are no longer visible. Because of the frequently intermittent nature of the entrapment, the horse should be examined on several occasions and preferably immediately after strenuous exercise. Radiography of the pharynx reveals the entrapped epiglottis.
Treatment consists of surgical revision of the aryepiglottic fold. However, given that the chronic condition has not been demonstrated to adversely affect performance, and that the complication rate for surgical correction of the disorder is 60%, careful consideration should be given to not attempting surgical repair, especially in animals performing to expectation.3 Entrapment associated with acute epiglottitis should include administration of antimicrobials and anti-inflammatory agents to resolve the epiglottitis.
This is usually a disease of racehorses, although animals of any age can be affected. The clinical signs are exercise intolerance, respiratory noise and coughing. The disease can readily be mistaken for epiglottic entrapment. The epiglottis is thickened and ulcerated, and these changes are apparent on endoscopic examination. Treatment includes topical application of a mixture of nitrofurazone, dimethyl sulfoxide, glycerin and prednisolone, and systemic administration of anti-inflammatory drugs. The prognosis for recovery is excellent.4
Fluid-filled cysts in the subepiglottic, dorsal pharyngeal or soft palate tissues cause exercise intolerance and abnormal respiratory noise in exercising adult horses and mild dysphagia, chronic cough and nasal discharge in foals.5,6 The cysts are usually embryonic remnants, although cysts may be acquired in adult horses by obstruction or inflammation of mucous glands.6 Endoscopic examination of the upper airway reveals the presence of smooth-walled cysts. Subepiglottic cysts may only be apparent on careful examination of the epiglottis, although most will cause the epiglottis to assume a more upright posture than is normal. Treatment is surgical removal.
This is a progressive disease of the arytenoid cartilages in which there is distortion of the cartilage with consequent partial occlusion of the lumen of the larynx. The cause of the disease is not known but it is most common in racehorses in heavy work.7 Distortion and swelling of the cartilage, combined with restricted abduction, increase resistance to airflow through the larynx and cause respiratory noise during exercise and exercise intolerance. In severe cases respiratory noise and increased respiratory effort may be apparent at rest. The disease can occur as a progression of idiopathic mucosal ulceration of the axial aspect of the arytenoid cartilages.8
Endoscopic examination reveals the cartilage to be enlarged and distorted and there may be luminal projections of cartilage and granulation tissue. In less severe cases there is mild swelling of the cartilage and ulceration of the mucosa covering the cartilage. Bilateral disease is uncommon. The cartilage contains areas of necrosis, dystrophic mineralization and granulation tissue.
Lesions of the mucosa of the axial aspect of the arytenoid cartilages are observed in Thoroughbred race horses.3,8 The condition occurs in approximately 2.5% of Thoroughbred race horses and 0.6% of Thoroughbred yearlings.3,8 The pathogenesis is unknown. The disorder is recognized during endoscopic examination of the horses for other reasons (before sale, examination for exercise-induced pulmonary hemorrhage). Endoscopic appearance of the lesion is that of a roughly circular lesion of the mucosa of the axial surface of the arytenoid cartilage, with or without visual evidence of inflammation, and without deformity of the underlying cartilage.8 The lesions can progress to arytenoid chondritis, although most do not.8 Because of the risk of progression, medical therapy including systemic or local administration of antimicrobial and anti-inflammatory drugs is indicated.8 The prognosis for full recovery is excellent.
This is one of the most common abnormalities detected during laryngoscopic examination of horses running on a treadmill.9 The disorder can only be detected in horses by endoscopic examination of the larynx while the horse is performing strenuous exercise. Collapse of the axial portion of the aryepiglottic folds causes obstruction of the laryngeal airway during inspiration. Treatment is by transendoscopic laser ablation of the portion of the fold that collapses during exercise.10
This uncommon cause of exercise intolerance and respiratory noise during strenuous exercise is detected during endoscopic examination of exercising horses.11 During exercise, the epiglottis of affected horses flips into the larynx during inspiration and back to its normal position during expiration. The cause is unknown but the condition can be induced by injection of local anesthetic around the hypoglossal and glossopharyngeal nerves.12 Treatment is rest.
Lymphadenopathy of the retropharyngeal lymph nodes is usually associated with S. equi var. equi infection and is often a sequel to strangles (see Strangles).13,14 Shedding of S. equi from clinically inapparent retropharyngeal lymph node abscesses is an important source of new infections in horse barns. Retropharyngeal lymphadenopathy is also caused by trauma to the pharynx and neoplasia (predominantly lymphosarcoma). Enlargement of the retropharyngeal lymph nodes compresses the nasopharynx, increases resistance to air flow and may impair swallowing.
Clinical signs are swelling of the parotid region, although this may be slight even in horses with marked respiratory distress, pain on palpation of the parotid region, stertorous respiratory noise, respiratory distress and dysphagia evident as food material discharging from the nostrils. Affected horses are frequently depressed, inappetent and pyrexic.
Endoscopic examination of the upper airway will reveal ventral displacement of the dorsal wall to the pharynx and narrowing of the nasopharynx. There may be deviation of the larynx to the side away from the mass. Guttural pouch empyema often coexists with retropharyngeal lymph node infection and the guttural pouches should be examined. Radiography will reveal the presence of a soft tissue density in the retropharyngeal region with compression of the guttural pouches and pharynx. Hematological examination often demonstrates a mature neutrophilia and hyperfibrinogenemia. The serum antibody titer to the M protein of S. equi is usually elevated.
Treatment consists of administration of penicillin (procaine penicillin 20 000 IU/kg, intramuscularly every 12 h) until signs of the disease resolve, followed by administration of a combination of sulfonamide and trimethoprim (15–30 mg/kg orally every 12 h for 7–14 d). Administration of anti-inflammatory drugs such as phenylbutazone (2.2 mg/kg intravenously or orally every 12 h) is important in reducing inflammation and swelling and thereby allowing the horse to eat and drink. Horses that have severe respiratory distress may require a tracheotomy. Dysphagic horses may require fluid and nutritional support. Surgical drainage of the abscess is difficult and should be reserved for cases with large, cavitating lesions evident on radiographic or ultrasonographic examination.
Control consists of preventing infection of horses by S. equi var. equi and adequate treatment of horses with strangles.
1 Boles C, et al. J Am Vet Med Assoc. 1978;172:883.
2 Sweeney CR, et al. J Am Vet Med Assoc. 1991;198:1037.
3 Brown JA. Equine Vet J. 2005;37:397.
4 Hawkins J, Tulleners EP. J Am Vet Med Assoc. 1994;205:1577.
5 Stick JA, Boles CL. J Am Vet Med Assoc. 1980;77:62.
6 Haynes PF, et al. Equine Vet J. 1990;22:369.
7 Haynes PF, et al. J Am Vet Med Assoc. 1980;177:1135.
8 Kelly G, et al. Equine Vet J. 2003;35:276.
9 Tan RH, et al. Vet J. 2004;170:243.
10 King DS, et al. Vet Surg. 2001;30:151.
11 Parente EJ, et al. Equine Vet J. 1998;30:270.
12 Holcombe SJ, et al. Equine Vet J Suppl. 1999;30:45.
The guttural pouches are diverticula of the auditory (or eustachian) tubes found in equids and a limited number of other species.1,2 The function of the guttural pouch is unclear, although it may have a role in regulation of cerebral blood pressure, swallowing, and hearing.1 It is unlikely to have a role in brain cooling.2 Each guttural pouch of an adult horse has a volume of approximately 300 mL and is divided by the stylohyoid bone into lateral and medial compartments.
The medial compartment of the guttural pouch contains a number of important structures including the internal carotid artery and glossopharyngeal, hypoglossal, and spinal accessory nerves in addition to branches of the vagus nerve and the cervical sympathetic trunk. Retropharyngeal lymph nodes lie beneath the mucosa of the ventral aspect of the medial compartment, an important factor in the development of guttural pouch empyema.
In the lateral compartment the external carotid artery passes along the ventral aspect as do the glossopharyngeal and hypoglossal nerves. Involvement of any of the above-mentioned structures is important in the pathogenesis and clinical signs of guttural pouch disease, and may result in abnormalities, such as Horner’s syndrome, that are not readily recognized as being caused by guttural pouch disease.
The common diseases of the guttural pouch are described below.
Empyema is the accumulation of purulent material in one or both guttural pouches. Initially, the purulent material is liquid, although it is usually viscid, but over time becomes inspissated and is kneaded into ovoid masses called chondroids. Chondroids occur in approximately 20% of horses with guttural pouch empyema.3 The condition is most commonly associated with S. equi var. equi infection and is a recognized sequel to strangles.3-5 Therefore, any horse with guttural pouch empyema should be isolated and treated as if it were infected with S. equi var. equi until proven otherwise. The empyema may be associated with other conditions of the guttural pouches, especially if there is impaired drainage of the pouch through the pharyngeal opening of the eustachian tube.
The epidemiology, apart from its association with strangles, has not been defined. The disease occurs in all ages of horses, including foals, and all equids, including asses and donkeys.3 The case fatality rate is approximately 10%, with one-third of horses having complete resolution of the disease.3 Guttural pouch empyema occurs in approximately 7% of horses with strangles.4 The recovery rate for horses with uncomplicated empyema treated appropriately is generally considered to be good, although the presence of chondroids worsens the prognosis.
The pathogenesis of guttural pouch empyema is unclear although when secondary to strangles it is usually due to the rupture of abscessed retropharyngeal lymph nodes into the medial compartment. Continued drainage of the abscesses presumably overwhelms the normal drainage and protective mechanisms of the guttural pouch, allowing bacterial colonization, influx of neutrophils and accumulation of purulent material. Swelling of the mucosa, especially around the opening to the pharynx, impairs drainage and facilitates fluid accumulation in the pouch. The accumulation of material in the pouch causes distension and mechanical interference with swallowing and breathing. Inflammation of the guttural pouch mucosa may involve the nerves that lie beneath it and result in neuritis with subsequent pharyngeal and laryngeal dysfunction and dysphagia.
These include:3
• Swelling of the area caudal to the ramus of the mandible and ventral to the ear
• Carriage of the head with the nose elevated above its usual position
The nasal discharge is usually unilateral, as is the disease, intermittent and white to yellow. Guttural pouch empyema is not usually associated with hemorrhage, although the discharge may be blood tinged. Bilateral disease, and the resultant neuritis and mechanical interference with swallowing and breathing, may cause discharge of feed material from the nostrils, dysphagia and respiratory stertor.
Endoscopic examination of the pharynx reveals drainage of purulent material from the pharyngeal opening of the eustachian tube of the affected side. The guttural pouch contains a variable quantity of purulent material, although in severe cases the quantity of fluid may be sufficient to prevent adequate examination of the pouch with an endoscope.
Radiographic examinations demonstrate the presence of radiodense material in the guttural pouch, sometimes the presence of an air–gas interface (fluid line) within the pouch and distension of the pouch with impingement into the nasopharynx.5 Chondroids are evident as multiple circular radiodensities. Passage of a catheter into the guttural pouch via the pharyngeal opening permits aspiration of fluid for cytology and bacterial culture.
Hematological examination may reveal evidence of chronic infection, including a mild leukocytosis, hyperproteinemia, and hyperfibrinogenemia. Fluid from the affected guttural pouch contains large numbers of degenerate neutrophils and occasional intracellular and extracellular bacteria. Bacterial culture yields S. equi in approximately 30% of cases and S. zooepidemicus in approximately 40% of cases.3
Lesions of guttural pouch empyema include the presence of purulent material in the guttural pouch and inflammation of the mucosa of the affected guttural pouch.
Diagnostic confirmation in a horse with clinical signs of guttural pouch disease is achieved by demonstration of purulent material in the guttural pouch by endoscopic or radiographic examination and examination of the fluid.
Differential diagnosis of guttural pouch empyema includes:
Guttural pouch empyema should also be differentiated from other causes of nasal discharge in horses including:
Infection by Mycobacterium avium complex organisms causes nasal discharge and granulomatous lesions in the guttural pouch.6
The principles of treatment are removal of the purulent material, eradication of infection, reduction of inflammation, relief of respiratory distress and provision of nutritional support in severely affected horses.
Removal of purulent material may be difficult but can be achieved by repeated flushing of the affected guttural pouch. The guttural pouch can be flushed through a catheter (10–20 French, 3.3–7 mm male dog urinary catheter) inserted as needed via the nares, or a catheter (polyethylene 240 tubing) with a coiled end inserted via the nares and retained in the pouch for several days.7 The pouch can also be flushed through the biopsy port of an endoscope inserted into the guttural pouch.
The choice of fluid with which to flush the guttural pouch is arbitrary but frequently used fluids include normal (isotonic) saline, lactated Ringer’s solution or 1% (v/v) povidone–iodine solution. It is important that the fluid infused into the guttural pouch be nonirritating as introduction of fluids such as hydrogen peroxide or strong solutions of iodine (e.g. 10% v/v povidone iodine) will exacerbate the inflammation of the mucosa and underlying nerves and can actually prolong the course of the disease.8 The frequency of flushing is initially daily, with reduced frequency as the empyema resolves.
Infusion of antibiotics into the guttural pouches is probably without merit. Because of the viscid nature of the empyema fluid, it is necessary to infuse large volumes of lavage solution (1–2 L) on consecutive days. It may be necessary to treat for 7–10 days. The infusion of acetylcysteine (60 mL of a 20% solution) into the pouch after lavage with 1–2 L of saline has been reported to be effective in aiding the removal of purulent material.9 Removal of chondroids usually requires surgery, although dissection and removal of chondroids through the pharyngeal opening has been described.10 A stone remover inserted through the biopsy channel of the endoscope can be useful for removal of small numbers of chondroids, but is tedious if there are large numbers of them. A rule of thumb is that if the chondroids occupy more than one-third of the volume of the guttural pouch, then removal should be carried out surgically.
Systemic antimicrobial administration is recommended for all cases of guttural pouch empyema because of the frequent association of the disease with bacterial infection and especially S. equi and S. zooepidemicus infection of the retropharyngeal lymph nodes.3 The antibiotic of choice is penicillin G (procaine penicillin G, 20 000 IU/kg intramuscularly every 12 h for 5–7 d), although a combination of sulfonamide and trimethoprim (15–30 mg/kg orally every 12 h for 5–7 d) is often used. Topical application of antimicrobials into the guttural pouch is probably ineffective because they do not penetrate the infected soft tissues of the pouch and retropharyngeal area.
NSAIDs such as flunixin meglumine (1 mg/kg intravenously or orally every 12 h) or phenylbutazone (2.2 mg/kg intravenously or orally every 12 h) are used to reduce inflammation and pain. Severely affected horses may require relief of respiratory distress by tracheotomy. Dysphagic horses may need nutritional support, including administration of fluids.
Chronic cases refractory to treatment might require fistulation of the guttural pouch into the pharynx.11
1 Baptiste KE. Vet J. 1998;155:139.
2 Maloney SK, et al. S Afr J Sci. 2002;98:189.
3 Judy CE, et al. J Am Vet Med Assoc. 1999;215:1666.
4 Sweeney CR, et al. J Am Vet Med Assoc. 1987;191:1446.
5 Newton JR, et al. Vet Rec. 1997;140:84.
6 Sills RC, et al. Vet Pathol. 1990;27:133.
7 White SL, Williamson L. Vet Med. 1987;82:76.
8 Wilson J. Equine Vet J. 1985;17:242.
9 Bentz BG, et al. Equine Pract. 1996;18:33.
10 Seahorn TL, Schumacher J. J Am Vet Med Assoc. 1991;199:368.
Mycosis of the guttural pouch is caused by infection of the dorsal wall of the medial compartment of the pouch, caudal and medial to the articulation of the stylohyoid bone and the petrous temporal bone.1 The most common fungi isolated from the lesions are Aspergillus (Emericella) nidulans, Aspergillus fumigatus and, rarely, Penicillium spp. and Mucor spp., although spores of these fungi are present in the guttural pouches of normal horses.2
The disease occurs in horses of both genders and all breeds. Horses are affected at all ages, with the youngest recorded case being a 6-month-old foal.3 The overall prevalence is low, although precise figures are lacking. The case fatality rate is approximately 33%.
The pathogenesis of the disease is unclear, although it is likely that fungal spores gain access to the guttural pouch through the pharyngeal opening. The spores then germinate and proliferate in the mucosa of the dorsal, medial aspect of the medial compartment of the guttural pouch. The location of the lesion is consistent but the reason for the disease occurring in this particular position is unclear. Factors that predispose to the development of mycotic lesions have not been determined, although it appears unlikely that fungal infection is the initial insult to the mucosa. Invasion of guttural pouch mucosa is followed by invasion of the nerves, arteries, and soft tissues adjacent to it. Invasion of the nerves causes glossopharyngeal, hypoglossal, facial, sympathetic or vagal dysfunction. Invasion of the internal carotid artery, and occasionally the maxillary or external carotid, causes weakening of the arterial wall and aneurysmal dilatation of the artery, with subsequent rupture and hemorrhage. Death is caused by hemorrhagic shock or, in horses with dysphagia, aspiration pneumonia or starvation.
Guttural pouch mycosis is usually unilateral, although in approximately 8% of cases there is erosion of the medial septum and spread of infection into the other pouch.4 There is no predisposition for either the left or right pouch.4 Guttural pouch mycosis presents as either epistaxis that is not associated with exercise or as cranial nerve disease.
Epistaxis is usually severe and frequently life-threatening. There is profuse bleeding of bright red blood from both nostrils during an episode, and between episodes there may be a slight, serosanguineous nasal discharge. There are usually several episodes of epistaxis over a period of weeks before the horse dies. Most horses that die of guttural pouch mycosis do so because of hemorrhagic shock.3,4
Signs of cranial nerve dysfunction are common in horses with guttural pouch mycosis and may precede or accompany epistaxis.
• Dysphagia is the most common sign of cranial nerve disease and is attributable to lesions of the glossopharyngeal and cranial laryngeal (vagus) nerves. Dysphagic horses may attempt to eat or drink but are unable to move the food bolus from the oral cavity to the esophagus
• Affected horses frequently have nasal discharge that contains feed material and often develop aspiration pneumonia
• Lesions of the recurrent laryngeal nerve cause laryngeal hemiplegia
• Horner’s syndrome (ptosis of the upper eyelid, miosis, enophthalmos and prolapse of the nictitating membrane) is seen when the lesion involves the cranial cervical ganglion or sympathetic nerve trunk
• Facial nerve dysfunction, evident as drooping of the ear on the affected side, lack of facial expression, inability to close the eyelids, corneal ulceration and deviation of the muzzle away from the affected side, also occurs.
Signs of cranial nerve and sympathetic trunk dysfunction may resolve with eradication of the infection, but are frequently permanent.4
Guttural pouch mycosis is also associated with pain on palpation of the parotid region, head shyness and abnormal head position. The infection may spread to the atlanto-occipital joint, causing pain on movement of the head,5 or to the brain, causing encephalitis.6
Endoscopic examination of the guttural pouch reveals a plaque of dark yellow to black necrotic material in the dorsal aspect of the medial compartment. A sample of the material can be collected through a biopsy port of the endoscope and submitted for culture. The mycotic plaque cannot be easily dislodged by manipulation with biopsy instruments or the end of the endoscope. In cases with ongoing or recent hemorrhage, the presence of large quantities of blood may prevent identification of the mycotic plaque. Both pouches should always be examined because of the occasional occurrence of bilateral disease or extension of the disease through the medial septum.
Radiographic examination of the guttural pouches may reveal the presence of a lesion in the appropriate position, but is frequently unrewarding.
There are no characteristic findings on the hemogram, nor are there serum biochemical abnormalities. Horses with repeated hemorrhage may be anemic. Immunoblot may identify the presence of serum antibodies specific for A. fumigatus in infected horses,7 although the diagnostic usefulness has not been determined. Culture of a sample of the necrotic tissue will frequently yield one of the causative fungi.
Lesions of guttural pouch mycosis include the presence of a clearly demarcated, yellow-brown to black, dry plaque of necrotic tissue in the dorsal aspect of the medial compartment of the guttural pouch. The plaque of tissue is firmly adherent to underlying tissues and may perforate the medial septum and invade the other pouch. The infection may involve the adjacent nerves and blood vessels and spread to soft tissues and bone. Histological examination reveals the presence of inflammatory cells in nerves and tissues surrounding the gross lesion. There is chromatolysis and degeneration of neurones in affected nerves. The internal carotid artery may have an aneurysmal dilatation or there may be rupture of the arterial wall without dilatation. There is usually partial thrombosis of the arterial wall.
Differential diagnoses for epistaxis not associated with exercise include ethmoidal hematoma or guttural pouch empyema, neoplasia, rupture of the longus capitis muscle8 or penetration by a foreign body.9
Treatment of guttural pouch mycosis involves prevention of death from hemorrhage and administration of antifungal agents.
Prevention of hemorrhage from the internal carotid or maxillary artery is achieved by surgical ligation, transarterial coil embolization or occlusion with intra-arterial balloons of one or more of the external carotid, internal carotid or maxillary artery.10,11 Because of the high rate of death from hemorrhage in horses with guttural pouch mycosis, some authorities recommend that all horses with the disease have the internal artery ligated or occluded.4,10 Medical treatment of horses with hemorrhage secondary to guttural pouch mycosis is rarely successful.10
Administration of antifungal agents by instillation into the guttural pouch through a catheter or endoscope has been reported, although there is disagreement about the need for such treatment in horses that have had the problematic arteries ligated or occluded.12 Oral administration of antifungal agents is generally ineffective or prohibitively expensive, although itraconazole (5 mg/kg orally once daily) may be useful.13 Agents reported to be usefully given by topical administration include enilconazole (60 mL of 33 mg/mL solution once daily for 3 weeks), miconazole (60 mL of 1 mg/mL solution), natamycin and nystatin.4,10,13 Topical therapy is laborious because it must be continued for weeks and involves placement and maintenance of a catheter in the guttural pouch, or instillation of medication by daily endoscopy.
Horses with signs of cranial nerve or sympathetic trunk damage may not recover completely even if cured of the fungal infection because of irreparable damage to the affected nerves. Provision of supportive care, including fluid and nutrient administration to dysphagic horses and administration of antibiotics to prevent or treat aspiration pneumonia, may be indicated.
1 Cook WR, et al. Vet Rec. 1968;83:422.
2 Blomme E, et al. Equine Vet Educ. 1998;10:86.
3 Cook WR. Vet Rec. 1968;78:396.
4 Greet TRC. Equine Vet J. 1987;19:483.
5 Walmsley JP. Equine Vet J. 1988;20:219.
6 Wagner PC, et al. Can Vet J. 1978;27:109.
7 Guillot J, et al. Am J Vet Res. 1997;58:1364.
8 Sweeney CR, et al. J Am Vet Med Assoc. 1993;202:1129.
9 Bayly WM, Robertson JT. J Am Vet Med Assoc. 1982;180:1232.
10 Lane JG. Equine Vet J. 1989;21:321.
11 Leveille R, et al. Vet Surg. 2000;29:389.
Guttural pouch tympany refers to the gaseous distension of one, rarely both, guttural pouches of young horses. Tympany develops in foals up to 1 year of age but is usually apparent within the first several months of life. Fillies are more commonly affected than are colts by a ratio of 2–4:1.1 The cause is not known although a polygenic cause has been proposed for Arabians.2
Clinical findings include marked swelling of the parotid region of the affected side with lesser swelling of the contralateral side. The swelling of the affected side is not painful on palpation and is elastic and compressible.3 There are stertorous breath sounds in most affected foals due to impingement of the distended pouch on the nasopharynx. Respiratory distress may develop. Severely affected foals may be dysphagic and develop aspiration pneumonia.
Endoscopic examination of the pharynx reveals narrowing of the nasopharynx by the distended guttural pouch. The guttural pouch openings are usually normal. There are usually no detectable abnormalities of the guttural pouches apart from distension. Radiographic examination demonstrates air-filled pouches, and dorsoventral images permit documentation of which side is affected. There are no characteristic changes in the hemogram or serum biochemical profile.
There are no characteristic lesions and necropsy examination usually does not demonstrate a cause for the disease.
Treatment consists of surgical fenestration of the medial septum allowing drainage of air from the affected pouch into the unaffected side. The prognosis for long-term resolution of the problem after surgery is approximately 60%.1
Rupture of the longus capitis muscle or avulsion of its insertion on the basisphenoid bone causes epistaxis and is usually associated with trauma to the head, such as is caused by rearing and falling over backwards.1 Endoscopic examination reveals:
• Compression of the nasopharynx that is asymmetric
• Submucosal hemorrhage and swelling of the medial aspect of the medial compartment of the guttural pouch.1
Radiographic examination reveals ventral deviation of the dorsal pharynx and loss of the usual radiolucency associated with the guttural pouch. Treatment is conservative and consists of supportive care, monitoring the hematocrit, and administration of broad-spectrum antibiotics if there is concern of the development of secondary infection. The prognosis for complete recovery is guarded.
Various neoplasms have been recorded as involving the guttural pouches. The presenting signs are: swelling of the parotid region, epistaxis, dysphagia or signs of cranial nerve disease. Neoplasms include melanoma, lymphosarcoma, hemangiosarcoma, squamous cell carcinoma and sarcoma.2 Diagnosis is made by physical, endoscopic and radiographic examination and biopsy. The prognosis is very poor to hopeless.
Primary congenital defects are rare in the respiratory tracts of animals. Hypoplasia of the epiglottis is detected occasionally in horses. Tracheal hypoplasia is recognized in calves and Miniature horses. Secondary defects, which are associated with major defects in other systems, are more common. Most of the defects in lambs are associated with defects of the oral cavity, face, and cranial vault.1 Accessory lungs are recorded occasionally2,3 and if their bronchi are vestigial the lungs can present themselves as tumor-like masses occupying most of the chest. Pulmonary hypoplasia is associated with congenital diaphragmatic hernia.