Synonym: Jaagsiekte
The very word “jaagsietke” denotes ‘driving disease’ amongst Africans due to the obvious reasons of the incidence of the disease in driven sheep. It is a vital chronic progressive pneumonic disease of sheep. The disease is characterized by proliferation of alveolar and bronchiolar epithelium resulting to increased respiratory distress, nasal discharge, coughing, emaciation and death.
Distribution
In 1904, Robertson and in 1915 Mitchell described about the disease in SOuth Africa as “Jaahsietke”. Dungal (1938) reported the disease in epizootic proportion and ascribed it as epizootic adenomatosis. Afterwards, the disease has been recorded in England, Peru, Greece, Germany, Kenya, Bulgaria, Italy. In India, Damodaran (1960) for the first time reported ovine pulmonary adenomatosis. Subsequently, the disease has been reported by various workers in different states of India.
Aetiology
The exact aetiology of the disease is not distinctly defined. The synergistic effects of two viruses have been suggested. The suggested viruses are herpes virus and retrovirus.
Susceptible Hosts
Sheep are primarily affected. Disease is most prevalent in older age group pf animals.
Mode of Transmission
A close association between healthy and diseased animal for a long period of time is required. This association is maximally possible during winter when the sheep are kept in close confinement. Experimental transmission of the disease by inoculation of lung materials through pulmonal or intravenous route is possible. Droplet infection through inhalation is suggested. Vertical transmission may occur.
Pathogenesis
Virus on entry multiply and localize in the lungs. There is development of adenomatous growth in the alveolar epithelium. As a result there is interference of oxygen exchange resulting to hypoxia and anoxia. Inflammatory and toxic reactions are absent.
Clinical Findings
There is prolonged incubation period. Animal shows respiratory dyspnoea, poor exercise tolerance and occasional coughing. There is emaciation, lachrymation and profuse serous discharge from both the nostrils. Lifting the animal by holding the hind quarter and keeping the head downward will show drainage of large quantity of water through both the nostrils. Moist rales may be heard from a distance. There is no depression of appetite and no appreciable rise of body temperature. Death usually ensues within 6 weeks to 16 weeks.
Lesions
The anterior and antero-ventral aspect of diaphragmatic lobes are mainly involved. The weight of the affected lobes are increased. The transformed tissues are firm but friable under pressure. The colour varies from greyish white to greyish red. Lungs display scattered firm greyish white nodules varying in size from just visible to one mm in diameter. Large nodules are due to fusion of several adjacent minute nodules. The nodules are usually surrounded by a pale area. The small nodules appear to bulge out from pleural surface.
Microscopically there is thickening of the inter-alveolar septa. This thickening is due to congestion and infiltration of mononuclear cells. Atelectasis of the alveoli leads to thickening of the inter alveolar septa. The adenomatous foci are multicentred and appear as compact glandular tissue separated by interalveolar wall adjacent to emphysematous alveoli. Alveolar epithelium shows metaplasia into tall columnar type and the alveolar spaces are completely occluded giving an appearance of fetalization of the lung parenchyma. Many cells show abundant cytoplasm with greatly enlarged ovoid or round nuclei. Flat cells of the alveoli undergo metaplastic changes into cuboidal cells supported by connective tissue. These metaplastic cells appear to grow in a pupillary manner into the alveolar space. Inter alveolar septa and connective tissue core of papilliform growth are thickened due to fibroblastic proliferation. Occasional, intracytoplasmic eosinophilic inclusion bodies are seen in cuboidal cells. In advance cases, the bronchial cells form papillary processes projecting to the bronchiolar and bronchial lumen. Fibroblastic proliferation is absent in early stages while in advanced stages, there is proliferation of fibroblasts.
Diagnosis
- Prolonged incubation period and characteristic lesions.
- Examination of nasal exudate – cluster of epithelial cells show hyperplastic adenomatous epithelium similar to alveolar epithelial cell.
- There is no reliable applicable laboratory tests but the following tests may be under taken like complement fixation test, agar gel diffusion test, ELISA.
Treatment
Treatment has got no bearance to alleviate clinical distress.
Control
- Slaughter of the affected animals and proper disposal of them.
- A formalized vaccine has given adequate response against the disease in sheep in Kenya. In India, no commercial vaccine is available at present and the incidence of the disease is seemed to be 1.44%
