Caseous Lymphadenitis

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Also known as: CLA

Introduction

This is a disease of sheep caused by the bacteria Corynebacterium ovis and C. pseudotuberculosis which are carried on the sheep skin. Infection is chronic and follows tissue trauma such as shearing wounds. Bacteria originate from ruptured lymph nodes in infected animals, and contaminate utensils and dipping fluids. Docking and castration wounds and the umbilicus are less frequent routes. Inhalation and ingestion are uncommon routes. The incubation period is around 3 months long.

Pathophysiology

These are non-nitrate-reducing biotypes of bacteria which survive in the environment for >6 months, especially in damp conditions. Inoculated bacteria are engulfed by phagocytic cells, proliferate intracellularly, and spread via lymphatics to regional lymph nodes. Bacterial proliferation occurs both intracellularly and extracellularly in lymph nodes. Lymph node enlargement occurs through alternating necrosis and reformation of the lesion capsule, causing distinctive laminated appearance of older lesions. In chronic infections, bacteria enter efferent lymphatics or blood vessels and spread to lungs, thoracic lymph nodes, or abdominal viscera (liver, kidney, spleen).

There are three bacterial virulence factors. These are heat-labile exotoxin (sphingomyelin-specific phospholipase D exotoxin), which causes decreases in erythrocyte membrane sphingomyelin content, and significant increases in phosphatidylglycerol (a glycerophospholipid). It also causes increased vascular permeability (due to sphingomyelinase activity on vascular endothelial cells). Phospholipase D exotoxin is the major bacterial virulence factor, and is responsible for primary infectivity and dissemination to regional lymph nodes. Secondarily, heat-stable pyogenic factor which is resistant to heat and formalin, and may enhance local lesions. Finally, leukotoxic surface lipid allows the organism to survive within inactivated macrophages, and also induces caseous necrosis.

In caseous lymphangitis, abscessation of superficial and internal lymph nodes may occur if there is haemtogenous spread. Infection is spread by pus from the abscesses and oculonasal secretions.

In sheep, disease commonly involves prescapular and inguinal lymph nodes. In goats, mandibular and parotid lymph nodes are most commonly affected. Multiple enlarged lymph nodes appear clinically as multiple subcutaneous nodules. In young animals, infection is typically confined to lymph nodes. Often there are no specific clinical signs in sheep affected with the visceral form of CLA. Progression to visceral disease is usually slow, and it typically affects older animals. Nodal abscesses may rupture and cause draining cutaneous fistulae. The disease may occasionally causes mastitis in sheep and often causes it in goats.

Signalment

Chronic suppurative infection of sheep, goats and occasionally cattle. It can occur at any age.


Clinical Signs

There will be signs of ill thrift and mild depression. Abscesses will be visible and they will be green in colour and have an onion ring appearance. Pneumonia may also occur. The disease in some rarer cases, may cause myositis. The visceral form of CLA is one of the factors associated with 'thin ewe syndrome'. The disease is rarely fatal and only seldom causes clinical signs and debilitation. Large pulmonary abscesses do occasionally cause fatalities. Rarely, small outbreaks of polyarthritis occur in lambs; affected animals generally recover spontaneously.

Diagnosis

Clinical signs can be indicative of the disease. Sandwich ELISA can be performed to detect circulating antibodies to phospholipase toxin.

Lesions are often seen as a coincidental finding at post mortem. In sheep lymph nodes are greatly enlarged and consist of central core of thick creamy necrotic material that is greenish-white, yellow, or tan, and gritty. Older lesions in sheep are characterized by concentrically laminated layers of fibrous connective tissue, with alternating zones of caseous, friable material (“onion skin”) that is entirely bounded by a thick fibrous capsule.

In goats, exudate is less dry and is not concentrically laminated or mineralized. Microscopic features include caseous necrosis of lymph nodes, with the intial lymph node lesion beginning as lymphadenitis, with the formation of multiple microscopic abscesses in the cortex. Eosinophils may predominate initially. Microabscesses rapidly coalesce, forming areas of caseation with bacteria. Abscesses become rapidly encapsulated by fibrous connective tissue, and the lymph node enlarges. With continued enlargement, there is progressive necrosis and mineralization of the parenchyma, with formation of calcareous granules deposited in successive layers with fibrous connective tissue.

The lymph node abscesses in goats may resemble melioidosis/pseudoglanders caused by Burkholderia (Pseudomonas) pseudomallei and this differential diagnosis will need to be excluded.

Treatment and Control

Importation measures form a part control strategy, including screening, culling of infected sheep, strict hygiene and administration of an inactivated vaccine. If the disease is diagnosed, antibiotic treatment and topical iodophore shampoo can be used to treat it.

References

Jones TC, Hunt RD, King NW: Diseases caused by bacteria. In: Veterinary Pathology, 6th ed., pp. 479-481, Williams & Wilkins, Baltimore, MD, 1997

Ellis JA, et al.: Local production of tumor necrosis factor-α in corynebacterial pulmonary lesions in sheep. Vet Path 32:68-71, 1995

McNamara PJ, Bradley GA, Songer JG: Targeted mutagenesis of the phospholipase D gene results in decreased virulence of Corynebacterium pseudotuberculosis. Mol Microbiol 12:921-930, 1994

Brogden KA, Engen RL: Alterations in the phospholipid composition and morphology of ovine erythrocytes after intravenous inoculation of Corynebacterium pseudotuberculosis. Am J Vet Res 51:874-877, 1990

Stoops SG, Renshaw HW, Thilsted JP: Ovine caseous lymphadenitis: Disease prevalence, lesion distribution, and thoracic manifestations in a population of mature culled sheep from Western United States. Am J Vet Res 45:557-561, 1984

Valli VEO: The hematopoietic system. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., vol. 3, pp. 238-240, Academic Press, San Diego, CA, 1993 Updated 2000 by: Ed Stevens, AFIP



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