Caseous lymphadenitis of sheep and goats primarily affects lymph nodes and internal organs, leading to abscess formation. The condition not only compromises animal health but also leads to significant economic losses due to reduced wool yield, carcass condemnation, and decreased productivity. The disease spreads through direct contact, shearing equipment, and contaminated environments, making biosecurity and control measures essential in managing outbreaks.
Etiology:
The causative agent of caseous lymphadenitis is Corynebacterium pseudotuberculosis, a Gram-positive bacterium. Strains isolated from sheep and goats form a genetically similar group, distinct from those affecting horses and cattle. Both groups secrete an exotoxin known as phospholipase D, a key virulence factor and immunodominant antigen that breaks down sphingomyelin in host tissues. Variations in toxin output may influence the severity of infection. The bacterium’s lipid-rich cell wall enhances its survival within host cells by resisting phagocytic destruction. While C. pseudotuberculosis also causes ulcerative lymphangitis in cattle and horses and contagious acne in horses, these are considered separate conditions due to their differing disease mechanisms and lack of association with caseous lymphadenitis
Epidemiology:
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Geographic Distribution:
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Found in all major sheep-rearing countries: Australia, New Zealand, South Africa, the Middle East, the Americas, the UK, and parts of Europe.
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First appeared in the UK and the Netherlands in the late 1980s due to imported infected goats.
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Became established in those regions, peaking in the UK around 1998 before declining.
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Host Susceptibility:
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Primarily affects sheep and goats.
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Sheep are more commonly affected than goats.
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Prevalence in Sheep:
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Infection increases with age.
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Another study reported that 26% of mature sheep had lesions at slaughter.
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In the UK, early outbreaks were linked back to a single introduction strain.
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Prevalence in Goats:
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Generally lower than in sheep.
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Around 8% prevalence in both domestic goats in the U.S. and feral goats in Australia.
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Infection rates rise with age, reaching up to 22% by 4 years.
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Diagnosis in goats is complicated by other abscess-causing bacteria like Trueperella pyogenes.
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Source and Spread:
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Infected animals are the main source.
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Spread occurs through:
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Discharges from ruptured lymph node abscesses.
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Nasal and oral secretions in animals with lung involvement.
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Environmental persistence:
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Up to 8 months in pus-contaminated soil.
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4 months in shearing sheds.
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2 months on hay, straw, and fomites.
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Moist, cool conditions increase bacterial survival.
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Remains infectious in sheep dips for at least 24 hours.
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Transmission:
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Entry into the Body:
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Infection commonly occurs through skin wounds, but the bacterium can also penetrate intact skin.
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Modes of Transmission:
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Direct contact with pus or secretions from infected abscesses.
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Contaminated shearing equipment, such as clippers or blades, acts as a major source.
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Surfaces in shearing sheds, holding pens, and equipment can harbor the bacteria.
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Contaminated dipping or shower fluids can facilitate spread between animals.
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Airborne dust particles in shearing sheds and yards may carry the organism, especially in dry and dusty conditions.
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Pathogenesis:
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Within 1 day of experimental skin infection, multiple microscopic abscesses form in the draining lymph nodes.
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By 3 to 10 days, these small abscesses merge into characteristic pyogranulomas, a hallmark of caseous lymphadenitis.
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The bacterium secretes an exotoxin (phospholipase D) that targets sphingomyelin in cell membranes, leading to increased vascular permeability and flooding of lymphatic channels, aiding bacterial spread.
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Abscesses occur in 60% to 80% of infected sheep, indicating high pathogenic potential.
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The lipid-rich bacterial cell wall resists breakdown by phagocytic enzymes, allowing the organism to survive and multiply within immune cells.
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Infected animals may experience reduced wool production in the first year due to the systemic effects of inflammatory cytokines and toxins released during the immune response.
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The pathogen can spread through the bloodstream (hematogenous spread), forming abscesses in internal organs, even in the absence of visible external lesions.
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Up to 25% of sheep at slaughterhouses have lesions confined to thoracic organs (e.g., lungs) without peripheral signs.
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Lung involvement is frequently reported, although prevalence varies based on geographic location and management practices.
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Other commonly affected internal areas include the abdominal organs and surrounding tissues.
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In rare cases, young lambs develop a septicemic form of the disease due to early systemic spread.
Clinical signs:
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Visible swelling is typically observed in one or more superficial lymph nodes, especially:
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Submandibular (under the jaw)
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Prescapular (shoulder region)
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Prefemoral (hind leg)
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Supramammary (near the udder)
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Popliteal (behind the knee)
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Over time, the infection may spread to other lymph nodes, either adjacent or systemic.
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In the UK, external abscesses in sheep are often located in the head and neck, but over 30% of affected sheep in one study had internal organ involvement without clear external signs.
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Both sheep and goats may develop skin abscesses, particularly on the face, which can result in hair loss over the lesion site.
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When the infection becomes systemic, it may manifest as:
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Chronic respiratory signs (e.g., pneumonia)
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Kidney inflammation (pyelonephritis)
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Nervous system issues like ataxia or hindlimb paralysis, depending on where abscesses form internally.
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A chronic wasting condition, often called “thin ewe syndrome”, is frequently linked to internal abscesses—with studies showing that 81% of affected ewes had such lesions and C. pseudotuberculosis present in 86% of those abscesses.
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Internal spread, especially from supramammary lymph nodes to the udder, can lead to:
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Decreased milk production
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Poor lamb growth or survival
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Major economic losses in severely affected flocks
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In rams, intrascrotal abscesses may develop, although these typically do not affect the testes or semen quality.
Differential diagnosis by :
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Melioidosis
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Tularemia
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Other causes of pneumonia in small ruminants
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Lymphosarcoma
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Suppurative lymphadenitis (Pasteurella multocida)
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Morel’s disease
Treatment:
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C. pseudotuberculosis is generally sensitive to antibiotics (except aminoglycosides), but treatment is rarely effective due to:
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Abscess encapsulation
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Intracellular persistence of the bacteria
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Surgical drainage or removal of external abscesses may be done in some cases.
Control Strategies:
Culling
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Removing animals with swollen lymph nodes helps reduce spread.
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Serological testing (e.g., ELISA) improves detection, especially for internal infections.
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This method may lead to high cull rates and may not be cost-effective without financial support.
Hygiene and Biosecurity
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Disinfect tools like ear-taggers, shears, and docking equipment before each use.
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Maintain cleanliness in shearing sheds and mobile trailers.
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Use farm-specific clothing for shearers and disinfect any pus-contaminated areas immediately.
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Shear sheep in order: young first, rams last, infected sheep at the end.
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Avoid crowding and contact after shearing.
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Prevent contamination of dipping fluid; one infected animal can contaminate the whole tank.
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In goats, avoid skin trauma by eliminating sharp objects and shared collars.
Vaccination
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Inactivated vaccines using phospholipase D reduce abscess formation and transmission.
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Vaccination reduces both the number and severity of abscesses.
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Full protocol: 2 doses in lambs + annual boosters = low infection rate (~3%).
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Partial protocols lead to much higher infection rates (up to 33%).
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Vaccination in goats shows limited success in natural settings.
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Colostral immunity can interfere with early vaccination; delay until 10 weeks in endemic flocks.
Eradication:
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Success reported through:
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Initial culling of symptomatic animals
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Repeated serological testing and removal of positives
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Strict biosecurity, disinfection of barns, and pasture rotation
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Lambs from positive ewes can be raised separately on cow’s milk.
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Some flocks achieved temporary disease-free status using repeated ELISA testing.
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Complete herd replacement is an option but carries a risk of reintroduction due to ELISA’s limited sensitivity (~90%).
Conclusion:
Caseous lymphadenitis remains a persistent threat to small ruminant health, especially in flocks and herds where control measures are inadequate. While complete eradication is challenging, integrated strategies such as vaccination, strict hygiene, routine serological testing, and responsible culling can significantly reduce disease prevalence. With timely intervention and improved awareness, the spread of CL can be controlled, ensuring better animal welfare and minimizing economic impact for farmers.
(FAQs)
Q1: What causes caseous lymphadenitis (CL)?
A1: CL is caused by Corynebacterium pseudotuberculosis, a bacterium that infects lymph nodes and internal organs in sheep and goats.
Q2: How is CL transmitted?
A2: Transmission occurs through direct contact with infected discharges, contaminated shearing tools, dips, or environments, especially when animals have skin wounds.
Q3: Can antibiotics cure CL?
A3: Antibiotic treatment is usually ineffective due to the encapsulated and intracellular nature of the bacteria. Surgical drainage may help with external abscesses.
Q4: Is there a vaccine for CL?
A4: Yes, inactivated vaccines are available and effective in reducing abscess development and disease spread, especially when used with proper booster protocols.
Q5: Can CL be eradicated from a flock?
A5: Yes, eradication is possible with rigorous culling, repeated serological testing, environmental sanitation, and controlled introductions, though it requires time and consistent effort.