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| + | == Introduction<br> == |
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| − | Caused by ''[[Corynebacterium ovis]]'' and [[Corynebacterium pseudotuberculosis|''C. pseudotuberculosis'']] carried on skin of sheep
| + | This is a disease of sheep caused by the bacteria ''[[Corynebacterium ovis]]'' and [[Corynebacterium pseudotuberculosis|''C. pseudotuberculosis'']] which is carried on the sheeps' 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 & ingestion are uncommon routes. The incubation period is around 3 months long.<br> |
| − | **Non-nitrate-reducing biotype
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| − | **Infection follows tissue trauma such as shearing wounds
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| − | **Incubation period 3 months
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| − | **Chronic suppurative infection of sheep, goats and occasionally cattle
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| − | **Abscessation of superficial and internal lymph nodes if haemtogenous spread occurs
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| − | **Caseous abscesses with green colour and onion ring appearance
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| − | **Ill thrift and pneumonia may occur
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| − | **Condemnation of carcasses and hides
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| − | **Infection spread by pus from abscesses, and oculonasal secretions
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| − | **Organism survives in environment for several months
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| − | **Sandwich ELISA detects circulating antibodies to phospholipase toxin
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| − | **Control: importation measures including screening; culling of infected sheep, stict hygiene; inactivated vaccine
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| − | *Ulcerative lymphangitis:
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| − | **Nitrate reducing biotype
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| − | **Disease in horses and cattle
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| − | **Infection through skin wounds
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| − | **Lymphangitis of lower limbs or abscessation in pectoral region
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| − | **Slow onset, usually becomes chronic
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| − | **Affected lymphatic vessels swollen and firm with nodules
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| − | **Oedema in affected limbs
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| − | **Ulcerative nodules exude thick green pus
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| − | **Lymphangitis and lymphadenitis in cattle with abscesses as well as coronary band lesions causing lameness
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| − | **Antibiotic treatment and topical iodophore shampoo
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| − | *May cause [[:Category:Bacterial Myositis|myositis]]
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| − | ''[[Corynebacterium ovis]]'' causes Caseous lymphadenitis
| + | 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. <br> |
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| − | GENERAL:
| + | In caseous lymphangitis, abscessation of superficial and internal lymph nodes if haemtogenous spread occurs. Infection is spread by pus fromthe abscesses and oculonasal secretions.<br> |
| − | *Disease is rarely fatal and seldom causes debilitation. Large pulmonary abscesses occasionally cause fatalities.
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| − | *Visceral form of CLA is one of the factors associated with “thin ewe syndrome".
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| − | *Rarely, small outbreaks of polyarthritis occur in lambs; affected animals generally recover spontaneously.
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| − | PATHOGENESIS:
| + | 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 typically affects older animals. Nodal abscesses may ruptures and cause draining cutaneous fistulae. The disease may occasionally causes mastitis in sheep and often causes it in goatss<br> |
| − | *Transmission occurs most often by wound infection, usually a shear wound in sheep. 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 & ingestion are uncommon routes.
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| − | *Bacteria survive in environment for >6 months, especially in damp conditions.
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| − | *Infection is reproduced experimentally by parenteral inoculation and through intact skin and mucous membranes.
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| − | *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.
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| − | *Lymph node enlargement occurs through alternating necrosis and reformation of the lesion capsule, causing distinctive laminated appearance of older lesions.
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| − | *In chronic infection, bacteria enter efferent lymphatics or blood vessels and spread to lungs, thoracic lymph nodes, or abdominal viscera (liver, kidney, [[Spleen - Anatomy & Physiology|spleen]]).
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| − | *There are three bacterial virulence factors:
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| − | a. Heat-labile exotoxin (sphingomyelin-specific phospholipase D exotoxin): Causes decreases in erythrocyte membrane sphingomyelin content, and significant increases in phosphatidylglycerol (a glycerophospholipid). 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.
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| − | b. Heat-stable pyogenic factor: Resistant to heat and formalin, and may enhance local lesions.
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| − | c. Leukotoxic surface lipid: Allows the organism to survive within inactivated macrophages, and also induces caseous necrosis.
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| − | CLINICAL FEATURES:
| + | <br> |
| − | *In sheep, disease commonly involves prescapular and inguinal lymph nodes.
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| − | *In goats, mandibular and parotid lymph nodes are most commonly affected.
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| − | *Multiple enlarged lymph nodes appear clinically as multiple subcutaneous nodules; in young animals, infection is typically confined to lymph nodes.
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| − | * Often there are no specific clinical signs in sheep affected with the visceral form of CLA. Progression to visceral disease is usually slow, and typically affects older animals. Nodal abscesses may ruptures and cause draining cutaneous fistulae.
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| − | *Mastitis occasionally occurs in sheep, and is often observed in goats.
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| − | GROSS LESIONS:
| + | == Signalment<br> == |
| − | *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.
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| − | *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.
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| − | *In goats, exudate is less dry and is not concentrically laminated or mineralized.
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| − | Laser disc: 892-95, 1380, 1500, 2915-17, 3046, 3298, 5416, 6424, 6427, 9287, 9422, 9492, 10142, 11569, 11658-59, 11678, 18557, 18938, 23548-50, 23636-37, 23651-52, 23775, 23779
| + | Chronic suppurative infection of sheep, goats and occasionally cattle. It can occur at any age. |
| − | Kodachromes: 9126, 9128
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| − | MICROSCOPIC FEATURES:
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| − | 1. Caseous necrosis of lymph nodes is the predominant feature.
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| − | 2. The initial lymph node lesion begins as lymphadenitis, with the formation of multiple microscopic abscesses in the cortex. Eosinophils may predominate initially.
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| − | 3. Microabscesses rapidly coalesce, forming areas of caseation with bacteria.
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| − | 4. 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.
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| − | DIFFERENTIAL DIAGNOSIS: The lymph node abscesses in goats may resemble melioidosis/pseudoglanders caused by Burkholderia (Pseudomonas) pseudomallei.
| + | == Clinical Signs<br> == |
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| − | COMPARATIVE PATHOLOGY (of C. ovis and other related corynebacteriae):
| + | 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 causes 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. |
| − | *C. ovis: Causes ulcerative lymphangitis and pectoral abscesses in horses, and rarely in cattle. Infection also reported in camels, deer, mules, and rarely humans.
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| − | *C. renale and C. pilosum: Pyelonephritis, ureteritis, and/or cystitis in cattle.
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| − | *C. cystitidis: Hemorrhagic cystitis and pyelonephritis in cattle.
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| − | *C. bovis: Rare cause of mastitis in cattle; cause of dermatitis in nude mice.
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| − | *C. suis (Eubacterium suis): Pyelonephritis and cystitis in swine.
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| − | *C. kutscheri: Pseudotuberculosis in rodents.
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| − | *C. ulcerans: Wound infections and abscesses in many species.
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| − | *Arcanobacter (Actinomyces) pyogenes: Suppurative infections in cattle, sheep, goats, and swine.
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| − | *Rhodococcus equi: Pneumonia and abscesses in foals and horses, and rarely in other species (cutaneous infections in cats).
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| − | *C. diphtheriae: Diphtheria in humans.
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| − | REFERENCES:
| + | <br> |
| − | 1. Jones TC, Hunt RD, King NW: Diseases caused by bacteria. In: Veterinary Pathology, 6th ed., pp. 479-481, Williams & Wilkins, Baltimore, MD, 1997
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| − | 2. Ellis JA, et al.: Local production of tumor necrosis factor-α in corynebacterial pulmonary lesions in sheep. Vet Path 32:68-71, 1995
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| − | 3. 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
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| − | 4. 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
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| − | 5. 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
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| − | 6. 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
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| − | Updated 2000 by: Ed Stevens, AFIP
| + | == Diagnosis<br> == |
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| | + | Clinical signs can be indicative of the disease. Sandwich ELISA can be performed to detect circulating antibodies to phospholipase toxin. |
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| − | [[Category:To_Do_-_Clinical]] | + | 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. 4. 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. |
| − | [[Category:Lymphoreticular and Haematopoietic Diseases - Sheep]] | + | |
| − | [[Category:Lymphoreticular and Haematopoietic Diseases - Goat]] | + | The lymph node abscesses in goats may resemble melioidosis/pseudoglanders caused by Burkholderia (Pseudomonas) pseudomallei and this differential diagnosis will need to be excluded. |
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| | + | == Treatment and Control == |
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| | + | Control measures include importation measures including screening; culling of infected sheep, stict hygiene; inactivated vaccine. If the disease is diagnosed, antibiotic treatment and topical iodophore shampoo can be used to treat.<br> |
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| | + | == References == |
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| | + | Jones TC, Hunt RD, King NW: Diseases caused by bacteria. In: Veterinary Pathology, 6th ed., pp. 479-481, Williams & Wilkins, Baltimore, MD, 1997 <br>Ellis JA, et al.: Local production of tumor necrosis factor-α in corynebacterial pulmonary lesions in sheep. Vet Path 32:68-71, 1995 <br>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 <br>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 <br>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 <br>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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| | + | [[Category:To_Do_-_Review]] [[Category:Lymphoreticular_and_Haematopoietic_Diseases_-_Sheep]] [[Category:Lymphoreticular_and_Haematopoietic_Diseases_-_Goat]] |