Difference between revisions of "Sheep Pulmonary Adenomatosis"

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[[Category:Respiratory_Viral_Infections]]
 
[[Category:Respiratory_Viral_Infections]]
 
[[Category:Respiratory Diseases - Sheep]]
 
[[Category:Respiratory Diseases - Sheep]]
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[[Category:Lungs - Pathology]]
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[[Category:Respiratory System - Hyperplastic/Neoplastic Pathology]]

Revision as of 17:54, 19 February 2011



Antigenicity

  • The virus cannot be grown in culture, although it can be seen by EM on tumor cells of infected sheep

Pathogenesis

  • Causes a proliferation of alveolar lining cells, producing massive amounts of fluid
  • Proliferative foci project into alveoli and bronchi and from slow-growing tumors
  • Death occurs between 3-4 years of age

Clinical signs:

  • Low exercise tolerance
  • Gradual weight loss
  • Dyspnoea
  • Coughing
  • Nasal fluid discharges during wheelbarrow test
  • Secondary bacterial infection by Pasteurella hemolytica often precipitates death
  • PM reveals fawn-gray tumor (for more see here)

Epidemiology

  • Found in 25% of pneumonia cases in Scotland
  • Absent in USA, common in UK

Diagnosis

  • Electron microscopy on lung biopsy

Control

  • Cull clinically affected animals



  • Also called pulmonary carcinomatosis
  • Infectious bronchiolar-alveolar carcinoma caused by a retrovirus
  • Commonest under intensive management systems which favour aerosol transmission and close contact of disease
  • Behaves like chronic pneumonia
  • Takes months to years to express itself clinically as coughing and exercise intolerance
  • Gross pathology:
    • Heavy lungs which fail to collapse
    • The lesions progress from small firm grey/white nodular lesions to extensive confluent areas with replacement by neoplastic tissue
    • Cut surface oozes fluid
    • There is often coexistent infection present
    • Occasional metastases to bronchial and mediastinal lymph nodes can occur
  • Histopathology:
    • Widespread proliferation of alveolar (Type 2) and terminal bronchiolar epithelium, lining the alveoli and lower airways
    • Multiple neoplastic foci of cuboidal/columnar cells forming papillary projections into the lumen
    • Metastases of the same in the bronchial and mediastinal lymph nodes
  • There is no serological test, and diagnosis depends upon raising the animal by the hind limbs whereupon a clear fluid issues from the nose = "Wheelbarrow test"

More information

Overview

Etiology: Type B/D Retrovirus (also known as the jaagziekte retrovirus‑‑JSRV)

Condition: Pulmonary carcinomatosis.

Synonyms: Jaagsiekte, sheep pulmonary adenomatosis, ovine pulmonary carcinoma.

General

  • Pulmonary carcinomatosis (OPC) is an infectious form of bronchioalveolar tumor with behavior of a low-grade carcinoma.
  • Associated with (and strong evidence that is caused by) a type B/D retrovirus of family Retroviridae (single-stranded RNA).
  • Occurs in Africa, Europe and the Americas.
  • Susceptibility among breeds varies; Merino sheep are highly susceptible.
  • The condition is considered to be a transmissible neoplasm with uncommon metastasis to regional lymph nodes and rare metastasis to other sites. Most growth is by local expansion and infiltration.
  • The disease spreads via aerosol transmission and is less common in areas where the sheep are dispersed.

Pathogenesis

  • The retrovirus associated with OPC is generally referred to as the jaagsiekte retrovirus (JSRV). This virus is morphologically distinct from all known retroviruses but has yet to be cultured.
  • The target cells are type II alveolar epithelial cells and, less frequently, nonciliated bronchiolar epithelium.
  • The virus-transformed epithelial cells proliferate, filling alveoli, spilling into adjacent airways and compressing and invading pulmonary parenchyma.
  • The exact mechanism of carcinogenesis is unknown.
  • Naturally occurring ovine pulmonary carcinomatosis has a long incubation period (months to up to 2 years), but experimentally, the time course of the disease can be reduced to a few weeks by inoculating lung tumor or lung fluid from affected sheep into neonatal lambs.

Clinical Signs

  • Coughing
  • Exercise intolerance (thus the Afrikaan name jaagsiekte, “driving sickness”).
  • Crackles and wheezes.
  • Abundant watery exudate which is discharged from the nose, especially when the head is lowered. The discharge is an important diagnostic clinical feature.
  • Dyspnea.

Findings

Gross Findings

  • Lung parenchymal masses ranging from 1 – 20 mm dia. gray-blue-white nodules (early) to large gray nodular and confluent masses (later). The larger masses often have fibrotic centers.
  • The lungs are enlarged, heavy, and fail to collapse.
  • Coexisting bronchopneumonia, verminous pneumonia, chronic progressive pneumonia, or combinations of the three.
  • Right ventricular hypertrophy and dilation.
  • Deaths result from heart failure, hypoxia or secondary bacterial pneumonias.

Laser Disc: 2395; 2396; 11702; 15547.

Microscopic Findings

  • Multiple proliferative foci of cuboidal or columnar cells which line alveoli and form papillary projections into their lumina (i.e., adenomatous hyperplasia, adenomas and adenocarcinomas).
  • In larger masses the pattern is obscured and fibroplasia often occurs in more disorganized and degenerative areas.
  • Early or uncomplicated lesions may have little to no accumulation of inflammatory cells; however, there are usually low to moderate aggregations of alveolar macrophages in alveolar lumina.

Ultrastructure

Some cells have cytoplasmic lamellar bodies characteristic of alveolar type II epithelial cells; others have secretory granules and glycogen compatable with secretory bronchiolar epithelial (Clara) cell origin.

Differential Diagnosis

  1. Chronic progressive pneumonia (maedi - lentivirus) --lymphofollicular interstitial pneumonia (with little to no significant alveolar epithelial hyperplasia).
  2. Remember, bacterial bronchopneumonias and verminous pneumonias may be present in addition to OPC.

Comparative Pathology

  • Human bronchio‑alveolar carcinoma shares many histologic and behavioral characteristics with OPC.
  • Type D retroviruses have been implicated in caprine and ovine nasal adenocarcinomas.

References

1. Hecht SJ, Sharp JM, and Demartini JC: Retroviral Aetiopathogenesis of Ovine Pulmonary Carcinoma: A Critical Appraisal. Br Vet J (1996) 152:395-406. 2. Dungworth DL: The Respiratory System, In:Pathology of Domestic Animals, 4th edition, ed. Jubb KVF, Kennedy PC, and Palmer N, pp.690-2, Academic Press, San Diego, CA, 1993. 3. Fenner FJ, Gibbs EPJ, Murphy FA, Rott R, Studdert MJ, and White DO: Retroviridae, In: Veterinary Virology, 2nd edition, pp. 578-9, Academic Press, Inc., San Diego CA, 1993. 4. Kimberling CV: Diseases of Adult Sheep, In: Jensen and Swift’s Diseases of Sheep, 3rd edition, pp. 270-3, 1988.

Written and revised by GD Young, 1988; BH Williams, 1991; WD Fall, 1994; TO Johnson, 1999.