Necrobacillosis

Veterinary Preventive Medicine I (MEDI-302), 3(3-0)

Dr. Zeeshan Ahmad Bhutta
Department of Clinical Sciences, Faculty of Veterinary Sciences,
Bahauddin Zakariya University, Multan, Pakistan
Introduction
• The term “necrobacillosis” commonly refers to infections associated
with necrotizing lesions caused by Fusobacterium necrophorum.
• Although oral necrobacillosis refers to an inflammatory process
affecting tissue of the oral cavity of calves, laryngeal necrobacillosis
refers to an infection of the more caudal pharyngeal and laryngeal
region.
• Calf diphtheria is a common synonym for necrobacillosis of the
pharynx and larynx, and necrotic stomatitis is a synonym for the oral
form.
ETIOLOGY
• F. necrophorum is a gram-negative, non–spore-forming, rod-shaped
anaerobic but aerotolerant organism.
• It is a normal inhabitant of the ruminant oral cavity and upper
digestive and respiratory tract and an opportunistic pathogen
generally associated with abscesses and various necrotic infections
• EPIDEMIOLOGY
• Occurrence
• The disease has no geographic limitations but is more common in
countries in which animals are housed in winter or maintained in
feedlots.
Epidemiology
• Transmission
• Oral/laryngeal necrobacillosis is an infectious but noncontagious
disease.
• The causative bacterium is a common inhabitant of the environment
and upper digestive tract of cattle.
• It has been proposed that the infection may be spread through dirty
milk pails and feeding troughs.
• Entry through the mucosa is probably affected through abrasions
caused by rough feed and erupting teeth.
Epidemiology
• Host Risk Factors
• Animals suffering from intercurrent disease or nutritional deficiency
are most susceptible
• Necrotic stomatitis is predominantly seen in weaned and unweaned
calves 2 weeks to 3 months of age.
• Laryngeal infections commonly affect older calves up to 1 year of age
and rarely occur in older animals up to 3 years of age.
• Pathogen Risk Factors
• LPS and leukotoxin (LT) Toxins
Pathogenesis
• F. necrophorum is a normal inhabitant of the oral cavity and causes
inflammation and necrosis once it is able to penetrate tissue, e.g., through
an injury of the mucosa of the oral cavity, pharynx, and larynx.
• Edema and inflammation of the mucosa of the larynx results in varying
degrees of closure of the rima glottidis and inspiratory dyspnea and stridor.
• The presence of the lesion causes discomfort, painful swallowing, and
toxemia.
• Extension of the lesion to the arytenoid cartilages will result in laryngeal
chondritis.
• Involvement of the cartilage will usually result in delayed healing or failure
to recover completely.
• The rima glottidis is the opening between the true vocal cords and
the arytenoid cartilages of the larynx.
Clinical Findings
• Laryngeal Necrobacillosis
• 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 Findings
• In calves affected with necrotic stomatitis, there is usually a moderate
increase in temperature (39.5°C–40°C; 103°F–104°F), depression, and
anorexia.
• The breath is foul and saliva, often mixed with straw, hangs from the
mouth.
• A characteristic swelling of the cheeks may be observed posterior to the lip
commissures, which, on opening the mouth this, is found to be caused by a
deep ulcer in the mucosa of the cheek.
• The ulcer is usually filled with a mixture of necrotic material and food
particles.
• An ulcer may also be present on the adjacent side of the tongue and cause
severe swelling and protrusion of the tongue.
• In severe cases the lesions may spread to the tissues of the face and throat
and into the orbital cavity.
Clinical Pathology
• Bacteriologic examination of swabs from lesions may assist in
confirming the diagnosis.
NECROPSY FINDINGS
• Severe swelling, caused by edema and inflammation of the tissues
surrounding the ulcer, is accompanied by the presence of large
masses of caseous material.
• Occasionally, lesions similar to those in the mouth, pharynx, and
larynx may be found in the lungs and in the abomasum.
• Microscopically, areas of coagulation necrosis are bordered by large
numbers of neutrophils and filamentous bacteria.
Samples for Confirmation of Diagnosis
• Bacteriology: anaerobic culture swab from deep within lesion
(ANAEROBIC CULT)
• Histology: formalin-fixed sample of interface between ulcer site and
normal tissue (light microscopy).
Treatment
• The lesions of necrotic stomatitis will usually heal in a few days
following debridement of the ulcers, application of a solution of
tincture of iodine, and oral administration of sulfamethazine at a dose
of 150 mg/kg BW daily for 3 to 5 days as labeled for use in food
animals, or parenteral penicillin or broadspectrum antimicrobials.
• Therapy should be at least for 5 days, and therapy for up to 3weeks
may be necessary.
• Corticosteroids may be a beneficial adjunctive therapy, especially to
reduce the edema.
• Tracheostomy may be necessary in some cases to relieve dyspnea.
Treatment
• Procaine penicillin (22,000 IU/kg IM every 12 h or 44, 000 IU/kg IM
every 24 h for at least 7 days)
• Oxytetracycline (10 mg/kg IM every 24h for at least 7 days or long-
acting formulation 20 mg/kg every 72 h)
• Ampicillin trihydrate (10 mg/kg SC or IM every 24 h for at least 7 days)
• Ceftiofur hydrochloride (2.2 mg/kg SC or IM every 24 h for at least 7
days)
• Dexamethasone (0.2–0.5 mg/kg IV or IM as a single dose)
Control
• Proper hygienic precautions in calf pens or feeding and drinking
places together with avoidance of rough feed should prevent the
spread of the disease.
• When the incidence is high, prophylactic antibiotic feeding may keep
the disease in check.
Any Question?