Necrotic stomatitis (oral necrobacillosis) is a serious infectious disease affecting the oral cavity of camelids (llamas, alpacas) and cervids (deer, elk, reindeer).
Overview and Clinical Importance
Necrotic stomatitis (oral necrobacillosis) is a serious infectious disease affecting the oral cavity of camelids (llamas, alpacas) and cervids (deer, elk, reindeer). The condition is characterized by necrotizing, ulcerative lesions of the oral mucosa caused primarily by Fusobacterium necrophorum, a gram-negative, obligate anaerobic bacterium. This disease represents a significant cause of morbidity and mortality in both domestic and wild populations of these species.
In camelids, necrotic stomatitis is relatively uncommon but can occur as part of a broader syndrome called alimentary necrobacillosis, which may involve the esophagus and gastric compartments. In cervids, the disease is more commonly recognized as part of the lumpy jaw complex or can present as primary oral lesions, particularly in farmed deer populations where it represents one of the most economically important diseases.
High-YieldF. necrophorum is a normal inhabitant of the gastrointestinal tract and requires mucosal damage to establish infection. On the NAVLE, always consider predisposing factors such as coarse feed, dental eruption, trauma, stress, or concurrent disease when presented with oral necrotic lesions.
| Subspecies |
Characteristics |
Clinical Relevance |
| subsp. necrophorum (Biotype A) |
More virulent; produces higher leukotoxin levels |
Primary cause of disease in animals; isolated more frequently from infections |
| subsp. funduliforme (Biotype B) |
Less virulent; lower leukotoxin production |
More commonly associated with human infections (Lemierre syndrome) |
Etiology
Primary Causative Agent
Fusobacterium necrophorum is the primary etiologic agent of necrotic stomatitis. Key characteristics include:
- Gram-negative, non-motile, non-sporulating, pleomorphic rod-shaped to filamentous bacterium
- Obligate anaerobe (aerotolerant-to-anaerobic)
- Normal inhabitant of the alimentary and urogenital tracts
- Does NOT penetrate healthy mucosa - requires breach in mucosal integrity
Subspecies
Virulence Factors
NAVLE TipRemember 'LEUKOTOXIN = LEUKOCYTE KILLER.' This is the MAJOR virulence factor that allows F. necrophorum to evade host defenses and establish infection. Studies in camelids have demonstrated leukotoxin in culture supernatants from all isolates.
Co-Infecting Agents
Necrotic stomatitis is often polymicrobial. Common co-infecting agents include:
- Trueperella pyogenes (formerly Arcanobacterium pyogenes) - synergistic relationship with F. necrophorum
- Actinomyces bovis - causes lumpy jaw; often concurrent in cervids
- Pseudomonas spp. - opportunistic; associated with environmental contamination
High-YieldT. pyogenes and F. necrophorum have a SYNERGISTIC relationship. T. pyogenes supplies a heat-labile factor that stimulates F. necrophorum replication, while F. necrophorum produces leukotoxin that aids T. pyogenes survival by killing immune cells.
| Virulence Factor |
Mechanism |
Clinical Effect |
| Leukotoxin |
Destroys polymorphonuclear leukocytes (PMNs) and macrophages |
Impairs host immune response; allows bacterial proliferation |
| Endotoxin (LPS) |
Induces inflammatory response and tissue damage |
Systemic signs; septicemia in severe cases |
| Hemagglutinin |
Promotes bacterial adhesion to host cells |
Facilitates colonization of damaged tissues |
| Dermonecrotic toxin |
Cell wall component causing tissue necrosis |
Characteristic coagulative necrosis with foul odor |
Pathogenesis
Disease Development Sequence
- Mucosal Damage: Initial breach in oral mucosa from trauma, coarse feed, dental eruption, or concurrent disease
- Bacterial Invasion: F. necrophorum colonizes damaged tissue; anaerobic environment created in wound favors growth
- Leukotoxin Production: Destruction of neutrophils and macrophages impairs local immune response
- Coagulative Necrosis: Extensive tissue necrosis with foul-smelling discharge; characteristic lesion formation
- Potential Spread: Bacteremia may lead to metastatic lesions in liver, lungs, or other organs
Predisposing Factors
| Camelidae |
Cervidae |
| Coarse or fibrous feeds (e.g., wheatgrass)
Chronic debilitating conditions
Neoplasia (GI adenocarcinoma)
Ingestion of caustic plants
Bezoars in gastric compartments
NSAID or glucocorticoid use |
Dental eruption (fawns)
Coarse feed causing oral abrasions
Overcrowding and stress
Poor sanitation/fecal contamination
Wet, muddy conditions
Social instability in herds |
Clinical Signs and Presentation
Camelidae (Llamas and Alpacas)
Clinical presentation in South American camelids includes:
- Anorexia and depression - often the first sign noticed
- Dysphagia - difficulty swallowing; drooling/ptyalism
- Halitosis - foul-smelling breath (characteristic)
- Oral lesions: Multifocal-to-coalescing ulcers on tongue, cheeks, and oral mucosa
- Weight loss - progressive emaciation
- Pyrexia - elevated temperature in acute cases
- Extension to GI tract - esophageal and gastric compartment involvement (C1, C2, C3)
Cervidae (Deer, Elk, Reindeer)
Clinical signs in cervids include:
- Swollen jaws or cheeks - 'lumpy jaw' appearance
- Necrotic oral lesions - ulcers with yellow-green purulent discharge
- Drooling and difficulty eating - feed dropping from mouth
- Weight loss and poor condition - dry coat, separation from herd
- Mandibular or maxillary swelling - hard, immovable masses at molar level
- Draining fistulous tracts - in advanced cases with abscess formation
NAVLE TipWhen you see 'lumpy jaw' in a deer on the NAVLE, think NECROBACILLOSIS first. Key distinguishing features: (1) FOUL ODOR - characteristic of F. necrophorum infections, (2) YELLOW-GREEN PUS - may contain sulfur granules, (3) BONE INVOLVEMENT - hard, immovable mass attached to jaw.
| Location |
Lesion Characteristics |
| Oral Mucosa |
Well-demarcated necroulcerative lesions; multifocal-to-coalescing ulcers; surrounded by hyperemic border; gray-yellow diphtheritic membrane |
| Tongue |
Bilateral ulcerated lesions at base; well-demarcated; localized lingual ulceration and necrosis |
| Cheeks |
Lesions near commissures of mouth; necroulcerative with foul odor; may extend to palate and gums |
| Jaw/Mandible |
Hard, bony swelling at molar level (lumpy jaw); abscesses with yellow-green pus; draining fistulas in advanced cases |
| Metastatic Sites |
Liver: hepatic abscesses; Lung: bronchopneumonia with nodules; forestomachs/rumen: mucosal necrosis |
Pathological Findings
Gross Lesions
Histopathological Features
- Coagulative necrosis - central necrotic core with amorphous debris
- Leukocyte destruction zone - rim of wholesale neutrophil destruction with dissipated nuclear chromatin
- Filamentous bacteria - concentrated at advancing edge of necrosis
- Peripheral hyperemia and hemorrhage - surrounding viable tissue shows severe vascular changes
- Local vessel thrombosis - common finding adjacent to necrotic foci
| Method |
Technique |
Findings |
| Clinical Exam |
Thorough oral examination; palpation of jaw and lymph nodes |
Necrotic lesions, foul odor, swelling; highly suggestive in cervids |
| Bacterial Culture |
Anaerobic culture on blood agar; incubate 24-48h at 37 degrees Celsius |
F. necrophorum isolation; often polymicrobial with T. pyogenes |
| Gram Stain |
Impression smears from lesions; Gram stain |
Slender gram-negative, rod-like or filamentous bacteria |
| PCR |
16S rDNA sequencing from lesion tissue; can use FFPE tissue |
Definitive identification; subspecies differentiation |
| Histopathology |
H&E staining of fixed tissue samples |
Coagulative necrosis; filamentous bacteria at necrotic margin |
| Radiography |
Survey radiographs of skull/jaw |
Bone involvement; osteolysis in chronic lumpy jaw |
Diagnosis
Diagnostic Approach
Differential Diagnosis
Exam Focus: Differentiate NECROBACILLOSIS (soft tissue necrosis, foul odor, F. necrophorum) from ACTINOMYCOSIS (bone involvement, slow-growing, A. bovis, sulfur granules) and ACTINOBACILLOSIS (soft tissue only, wooden tongue, A. lignieresii). These three conditions can occur concurrently!
| Condition |
Distinguishing Features |
| Vesicular Stomatitis |
Vesicles/blisters precede ulcers; may affect feet and teats; reportable disease |
| Contagious Ecthyma (Orf) |
Proliferative crusty lesions on lips; parapoxvirus; can occur concurrently |
| Actinomycosis (True Lumpy Jaw) |
Caused by Actinomyces bovis; sulfur granules; primarily bone involvement; chronic slow progression |
| Actinobacillosis (Wooden Tongue) |
Actinobacillus lignieresii; affects soft tissues not bone; tongue swelling and protrusion |
| Bottle Jaw (Arterial Worm) |
Caused by Elaeophora schneideri; submandibular edema; food impaction; primarily in deer |
| Oral Neoplasia |
Squamous cell carcinoma common in camelids; progressive; may have concurrent necrobacillosis |
Treatment
Antimicrobial Therapy
Early treatment is critical - once lesions become established with abscess formation, response to therapy is poor.
Note: Most drugs are NOT licensed for use in camelids or cervids. Consult with a veterinarian for extra-label drug use guidance.
Supportive Care
- NSAIDs: Flunixin meglumine (1.1 mg/kg IV) or meloxicam for pain and inflammation
- Local wound care: Debridement of necrotic tissue; flush with dilute iodine or chlorhexidine
- Abscess drainage: Lance and drain abscesses; flush cavity; may need repeated treatment
- Nutritional support: Soft feeds; ensure adequate hydration; may need assisted feeding
- Isolation: Separate affected animals to prevent environmental contamination
Surgical Intervention
For advanced cases with significant bone involvement:
- Surgical debridement of necrotic bone
- Curettage of mandibular/maxillary abscesses
- Combined with prolonged antimicrobial therapy
High-YieldTreatment failure is common in necrobacillosis, NOT because the bacteria are resistant, but because ABSCESSES have a protective membrane that prevents antimicrobial penetration. This is why EARLY treatment before abscess formation is crucial, and why surgical drainage is often necessary.
Prognosis
| Drug |
Dose |
Route/Freq |
Notes |
| Penicillin G |
22,000 IU/kg |
IM q24h x 5-7 days |
First-line; effective against F. necrophorum |
| Oxytetracycline |
6.6-11 mg/kg IV or 20 mg/kg IM (LA) |
q24h or single LA injection |
Good efficacy; can use prophylactically |
| Florfenicol |
20 mg/kg |
IM q48h |
Broad spectrum; good tissue penetration |
| Metronidazole |
15-25 mg/kg |
PO q12h |
Excellent anaerobic coverage; combines well with penicillin |
| Ceftiofur |
2.2-6.6 mg/kg |
IM/SC q24h |
Third-gen cephalosporin; broad spectrum |
Prevention and Control
Management Strategies
NAVLE TipVaccination against necrobacillosis has been attempted but has NOT demonstrated proven efficacy. The bacteria that cause this disease do NOT survive well in the environment, so environmental management and preventing the CONDITIONS for infection (mucosal damage, stress, contamination) are the key prevention strategies.
Zoonotic Considerations
F. necrophorum can rarely be transmitted to humans from handling animals with open sores or pus. In humans, F. necrophorum can cause:
- Lemierre syndrome - post-anginal septicemia with jugular vein thrombophlebitis
- Pharyngitis, peritonsillar abscess
- Skin and soft tissue infections
Always wash hands and exposed skin areas with soap and disinfectant after working with infected animals. Use appropriate PPE.
| Stage |
Prognosis |
| Early/Localized |
GOOD - Prompt antimicrobial therapy typically effective; lesions may heal with scarring |
| Established Abscess |
GUARDED - Requires surgical intervention plus prolonged antibiotics; may recur |
| Bone Involvement |
POOR - Bony changes are NOT reversible; chronic management or humane euthanasia |
| Systemic/Metastatic |
GRAVE - Septicemia with hepatic/pulmonary involvement usually fatal |
Memory Aids and Board Tips
FUSO Mnemonic for Necrotic Stomatitis
F = FOUL odor (characteristic halitosis)
U = ULCERATIVE, necrotic lesions
S = SECONDARY to mucosal damage (never primary infection)
O = OBLIGATE anaerobe (Fusobacterium necrophorum)
The 'LUMPY' Memory Aid for Cervid Necrobacillosis
L = Lesions at molar level
U = Ulcers with yellow-green pus
M = Mandibular swelling (hard, immovable)
P = Poor response if bone involved
Y = Young animals (fawns) especially susceptible during dental eruption
| Strategy |
Implementation |
| Feed Management |
Avoid coarse, fibrous, or stemmy feeds that can cause oral trauma; use soft bedding materials; remove foreign objects animals might chew |
| Hygiene |
Clean and disinfect feeding/watering equipment; prevent fecal contamination; use separate equipment for manure handling |
| Environmental |
Reduce wet, muddy conditions; replace contaminated soil near feeding areas with limestone; frequent bedding replacement |
| Stress Reduction |
Avoid overcrowding; minimize handling stress; maintain stable social groups; separate aggressive animals |
| Isolation |
Promptly isolate affected animals; collect and incinerate discharge/pus; do not allow pen contamination |
| Surveillance |
Daily observation for early signs; examine animals during feeding for problems eating, drooling, or weight loss |