Gross appearance is that of enlarged wet lungs, the interlobular septa are markedly widenedith oedema and emphysema
Underlying pathogenesis is ingestion of L-tryptophan in the pasture which is metabolised to 3-methylindole -> bloodstream -> lungs -> metabolised into a compound toxic to Type 1 pneumonocytes and non-ciliated bronchiolar epithelium
Their loss allows massive flooding of the alveoli with a protein-rich fluid
The sequence of events in the lung is as follows:
Alveolar flooding with a protein-rich fluid due to the necrosis of Type 1 epithelium
As the incoming air dries this fluid, fibrinous 'hyaline membranes' form
Proliferation of the more resistant cuboidal Type 2 epithelium which line the alveoli, called 'epithelialisation'
Then either there is
Digestion of the hyaline membranes by macrophages which when completed, allows some of the proliferated Type 2 epithelium to differentiate into Type 1 and reconstitute the functional respiratory unit - a normal alveolus
Or
Organisation of the fibrin into fibrous tissue in the lumen - destroying the alveolus or proliferation of fibrous tissue in the alveolar wall with retention of the epithelialised appearance to the alveolus
Sequel
Residual scarring if animal survives initial onslaught
In chronic exposures there may be extensive fibroplasia
Ingestion of sweet potatoes ifested with Fusarium solani mould or pasture contaminated with stinkweed or purple mint, rapeseed and kale also cause pulmonary oedema, emphysema and interstitial pneumonia
