History
A 5-year-old female alpaca was evaluated at the University of Georgia Veterinary Medical Teaching Hospital because of worsening respiratory difficulty of approximately 36 hours' duration. The alpaca had been treated with flunixin meglumine, diphenhydramine, and an antimicrobial prior to referral with no response. The alpaca was in the fourth month of gestation and had no history of previous medical problems. All other alpacas in the herd were reportedly healthy.
On initial evaluation, the alpaca was in respiratory distress with pronounced inspiratory stridor. An emergency temporary tracheostomy was performed, after which the respiratory effort and rate improved markedly. Thereafter, the alpaca had a rectal temperature of 40.1°C (104.1°F), heart rate of 52 beats/min, and respiratory rate of 36 breaths/min. Cardiothoracic auscultation revealed increased bronchovesicular sounds and intermittent wheezes referred from the upper airway. No cardiac abnormalities were found on auscultation. Contractions of the first forestomach compartment were decreased in frequency and intensity. The alpaca was thin (body condition score, 3/10) and weighed 61.4 kg (135 lb). A CBC and plasma biochemical analysis revealed hyperfibrinogenemia (700 mg/dL; reference range, 100 to 400 mg/dL) and hyperglycemia (207 mg/dL; reference range, 88 to 166 md/dL). Differential diagnoses considered for upper respiratory tract obstruction included edema, trauma, hematoma, abscess or granuloma formation, neoplasia, foreign body, and a functional laryngeal abnormality. Radiography of the pharyngeal and laryngeal region was performed (Figure 1).
Radiographic Findings and Interpretation
Most of the margins of the normal laryngeal structures are silhouetted by a well-defined soft tissue opacity (Figure 2). Two small mineral opacities are evident in this same region. A small volume of gas is present summating with the soft tissues over the midcervical portion of the trachea, consistent with prior placement of a tracheostomy tube. On the basis of the radiographic findings, the differential diagnoses considered most likely were an abscess or granuloma involving the laryngeal cartilages.
Treatment and Outcome
Upper airway endoscopy revealed marked enlargement of the left arytenoid cartilage with a normal-appearing right arytenoid cartilage. Furthermore, endoscopic examination revealed a complete inability to abduct the laryngeal cartilages bilaterally while breathing, an abnormality likely due to chronic inflammation with resultant paresis. The laryngeal opening was narrowed considerably, allowing only minimal airflow.
A diagnosis of left arytenoid chondritis was made. Medical management with antimicrobials and flunixin meglumine (1.1 mg/kg [0.50 mg/lb], IV, q 24 h) was attempted for 10 days, but arytenoid enlargement persisted and there was little clinical improvement. Surgical debridement of the left arytenoid cartilage through a laryngotomy was performed with the patient under general anesthesia, and full resolution of the condition was achieved. The patient remained hospitalized for 10 days following the surgical procedure, during which time treatment with antimicrobials, anti-inflammatories, and gastroprotectants was provided. Fetal viability was monitored serially with transabdominal ultrasonography. The patient was discharged from the hospital 3 weeks following initial evaluation.
Comments
Arytenoid chondritis is an uncommon cause of upper respiratory obstruction in New World camelids. Commonly referred to as calf diphtheria, the disease is common in cattle 3 to 18 months of age and usually affects animals in feedlots or housed at high stocking densities in unsanitary conditions.1 An abattoir study2 of cattle from feedlots demonstrated an incidence of approximately 1.7%, with most cases occurring during the winter months. The organism most commonly associated with arytenoid chondritis in cattle is Fusobacterium necrophorum, a gram-negative anaerobe. Fusobacterium necrophorum will not colonize intact mucous membranes, and therefore, laryngeal mucosal erosions caused by common respiratory viruses and persistent coughing or vocalization are required for the development of arytenoid chondritis.1 In horses, arytenoid chondritis has been most commonly described in young Thoroughbred and Standardbred racehorses, although the disease is also recognized in older horses of other breeds.3 The etiology of equine arytenoid chondritis is unknown, but mucosal trauma due to concussion of the opposing cartilages or inhaled foreign objects is suggested.4 Extension of infections from other locations within the respiratory tract might also play a role.5 Clinical signs typically include exercise intolerance and an inspiratory noise during exercise due to the decreased airway diameter; however, severely affected horses can be dyspneic at rest.3,5 A combination of medical and surgical treatments is usually required for resolution, but prognosis is often guarded for complete recovery in affected horses.3,5
Endoscopic examination of the upper airway and radiography of the pharynx and larynx are the diagnostic modalities of choice. Radiographs of the pharyngeal and laryngeal region are used to rule out other causes of airway disease, detect the presence of airway compression or stenosis, and determine the extent of laryngeal narrowing. If pneumonia secondary to aspiration is suspected, radiography of the thorax should be performed to document the extent of pulmonary involvement.6 In the alpaca of the present report, radiography of the larynx revealed marked soft tissue enlargement and mineralization of the laryngeal tissues, findings suggestive of arytenoid chondritis. Mineralization of the soft tissues was considered to be a dystrophic inflammatory change, suggestive of a chronic lesion. No other lesions associated with the upper respiratory tract were found. The prognosis for arytenoid chondritis in cattle is guarded. Medical treatment can be attempted and requires aggressive antimicrobial treatment with compounds effective against F necrophorum. In addition, anti-inflammatory medications are often required to manage inflammation and swelling. However, medical treatment is often unsuccessful and surgical debridement of the lesion or partial arytenoidectomy is required to achieve full resolution.7
1. Milne MH. Necrotic laryngitis. In: Kahn CM, Line S, Aiello SE, eds.The Merck veterinary manual. Hoboken, NJ: Merck, Sharp, and Dohme Corp, 2005.
2. Jensen R, Lauerman LH & England JJ, et al. Laryngeal diphtheria and papillomatosis in feedlot cattle. Vet Pathol 1981;18:143–150.
3. Ainsworth DM, Cheetham J. Arytenoid chondritis. In: Reed SM, Bayly WM, Sellon DC, eds.Equine internal medicine. St Louis: Saunders Elsevier, 2010;305.
4. Smith RL, Perkins NR & Firth EC, et al. Arytenoid mucosal injury in young Thoroughbred horses—investigation of a proposed aetiology and clinical significance. N Z Vet J 2006;54:173–177.
5. Haynes PF, Snider TG & McClure JR, et al. Chronic chondritis of the equine arytenoid cartilage. J Am Vet Med Assoc 1980;177:1135–1142.
6. Lakritz J, Rings DM, Hull BL. Disorders of the upper respiratory tract in food animals. In: Anderson DE, Rings DM, eds.Current veterinary therapy food animal practice. St Louis: Saunders Elsevier, 2009;199–207.
7. Nichols S, Anderson DE. Subtotal or partial unilateral arytenoidectomy for treatment of arytenoid chondritis in five calves. J Am Vet Med Assoc 2009;235:420–425.