Necrotic Laryngitis in Cattle

Predisposing factors are not fully understood. F necrophorum, commonly isolated from laryngeal lesions of affected cattle, is unable to penetrate intact mucous membranes. Laryngeal contact ulcers, a common finding in slaughtered cattle, are thought to provide a portal of entry for F necrophorum.

Necrotic laryngitis is most common where cattle are closely confined under unsanitary conditions or in feedlots. The prevalence in feedlot calves is estimated to be 1%–2%. Most cases are sporadic and occur year round, but disease peaks in fall and winter. Mixed upper respiratory tract infections (caused by infectious bovine rhinotracheitis virus and parainfluenza-3 virus; Mycoplasma spp; and bacteria, including Pasteurella and Haemophilus), and the coughing and swallowing associated with these infections, may predispose feedlot cattle to develop laryngeal contact ulcers. These ulcers on the vocal processes and medial angles of arytenoid cartilages are thought to provide a portal of entry for F necrophorum.

F necrophorum causes inflammation, necrosis, and edema in the laryngeal mucosa, resulting in variable narrowing of the rima glottidis and inspiratory dyspnea and stridor. If infection extends into the laryngeal cartilage, laryngeal chondritis develops, which may lead to a chronically deformed larynx. Pharyngeal invasion by the organism causes discomfort characterized by painful swallowing motions. Systemic signs of illness have been attributed to the exotoxin produced by F necrophorum.

Initially, a moist, painful cough is noticed. Severe inspiratory dyspnea, characterized by open-mouth breathing with the head and neck extended, and loud inspiratory stridor are common findings. Ptyalism; frequent, painful swallowing motions; bilateral, purulent nasal discharge; and a fetid odor to the breath may also be present. Systemic signs may include fever (106°F [41.1°C]), anorexia, depression, and hyperemia of the mucous membranes. Untreated calves die in 2–7 days from toxemia and upper airway obstruction. Longterm sequelae include aspiration pneumonia and permanent distortion of the larynx, resulting in a chronic harsh cough and inspiratory dyspnea.

Clinical signs are usually sufficient to establish a diagnosis. However, because numerous other conditions can cause signs of upper airway obstruction, the larynx should be visually inspected to confirm a diagnosis. This can be accomplished by means of an orally inserted speculum, laryngoscopy, endoscopy, or radiography, but care must be exercised to avoid further respiratory embarrassment. A tracheostomy should be performed before laryngoscopic or endoscopic examination in cattle with severe inspiratory dyspnea. Differential diagnoses include pharyngeal trauma; severe viral laryngitis (eg, infectious bovine rhinotracheitis); actinobacillosis; and laryngeal edema, abscesses, trauma, paralysis, or tumors.

Oxytetracycline (11 mg/kg, IV or SC, bid, or 20 mg/kg of long-acting tetracycline, SC, every 72 hr) or procaine penicillin (22,000 U/kg, IM, bid) are the antimicrobials of choice. NSAIDs (aspirin, 100 mg/kg, PO, bid; flunixin, 1.1–2.2 mg/kg, IV, once daily or divided bid; or ketoprofen, 3 mg/kg/day, IM or IV, for up to 3 days) are used to decrease the fever and laryngeal inflammation and edema. A single dose of dexamethasone (0.2–0.5 mg/kg, IV or IM) may be used to decrease laryngeal edema in animals with severe respiratory distress. A tracheostomy is indicated in cattle with severe inspiratory dyspnea. Good nursing care should be provided. Intravenous fluids may be required in dehydrated animals. The prognosis is good for early cases treated aggressively; chronic cases require surgery under general anesthesia to remove necrotic or granulation tissue and to drain laryngeal abscesses. A 60% success rate has been reported for surgical intervention in advanced cases.

There are no specific control measures for necrotic laryngitis; however, the proposed pathogenesis suggests that control measures for common respiratory pathogens may be beneficial.