AIP in the Feedlot

AIP in the Feedlot

AIP is the acronym for Acute (or Atypical) Interstitial Pneumonia. \"\" This disease is known by various different names over the years, such as Acute Bovine Pulmonary Emphysema and Edema, Bovine Asthma, Feedlot Dust Pneumonia, Fog Fever and the list goes on.



It is a primary respiratory disease that leads to severe edema and emphysema of the lung tissue that leads to death in the majority of cases. This is documented to be the second most important respiratory disease affecting feedlot cattle.

The financial impact of AIP can be significant, since it normally affects cattle in the finishing stage of their feeding period, animals which by that time increased in value to the producer due to increased weight – the result of various costly inputs.

Outside the feedlot setting, AIP is reported (often as outbreaks) on lush green pastures and fermented crops. Especially when moving animals from low quality roughage, to high quality pasture that have high protein levels. With a sudden increase in protein levels, L-Tryptophan (a common amino acid/or protein building block) is converted to 3-Methylindole (3-MI) in the rumen by bacterial species such Lactobacillus. 3-MI is then readily absorbed through the rumen into the bloodstream, and when it reaches the lungs it gets converted to 3-Methyleneindolenine (3-ME) and this molecule is then responsible for causing the damage to the lungs seen in AIP. 


The above description is accepted as the etiology for Fog Fever. In the feedlot setting however, there are no sudden change to lush green pastures as d\"\"escribed above, but 3-MI are still proposed to play a role in the feedlot AIP as well.

It is important to note that it is more a condition, than a specific disease, which means various different predisposing factors can lead to an animal developing AIP. These predisposing factors can be put into two categories namely dietary- and hypersensitivity types. The dietary form of AIP is then well described above, which involves sudden increases in feed with high levels of Tryptophan. Hypersensitivity AIP can develop as a result of various stressors, such as dust, dusty feed, moldy feed or bronchopneumonia.

In feedlot AIP the original cause is difficult to determine, but 3-MI is still suspected to have an effect in feedlot animals, and empirical evidence clearly shows that dust play a major role in precipitating the disease. A lot of the affected animals show a concurrent bronchopneumonia as well, which suggest the possible role as predisposing factor.

AIP mortality in feedlots usually increases in spring time when the wind and dust becomes a problem, and then quiet down when the rainy season arrives. Dust as mentioned above is a respiratory irritant that can lead to an allergic reaction in the lungs.

Heavy winds (which is common at this time of the year) often leads to aberrant feeding patterns and digestive disturbances, which can also predispose animals to AIP.

Temperature shifts are also a feature of South African spring time, which also suppress cattle immunity and resistance to disease.

It is also interesting to note that heifer calves are more prone to developing AIP than bull calves.Due to the fact that this disease coincides with wind and dust in the feedlot setting, feedlot managers often refer these lungs on post mortem \"\"as “dust lungs” or “wet lungs”, which describes the edema and emphysema that involve the whole lung in most cases.

The clinical picture of these animals is often that of animals that developed rapid respiratory disease. Severe dyspnea and panting is usually followed by death. Treatment success of these animals is very unrewarding and 30—50% mortality for animals that develop AIP is the norm.

On post mortem the lungs are usually dark red (sometimes marbled), enlarged and firm with a rubbery feel, and they do not collapse when cut. On the cut surface the lung tissue seems filled with fluid and air, the lungs are heavy with fluid when picked up, and have a shiny appearance. A definitive diagnosis can be made on histopathology when formalinized lung samples are submitted for examination. 

Various treatments have been proposed, but none with any dramatic effect. The current recommendation is to give an antibiotic as well as an anti-inflammatory drug as one would for infectious pneumonia. It is very important to train feedlot personnel to move these animals very slowly, since they are in severe respiratory distress. Note that they can even become aggressive due to their panic of not being able to breathe.  

Evidence suggests that a lot of AIP animals have concurrent pneumonia, which warrants the suggested treatment. Ancillary therapy with drugs like atropine or antihistamine has shown no beneficial effect. Emergency slaughter is often the best option.


Preventative measures can be implemented to try and lower the risk of feedlot cattle developing AIP. These can include reducing dust exposure in the feedlot. Sprinkler systems (mounted or mobile) have been used with great success to reduce dust where water is available. Stocking density, feedlot design and management can all play a role in reducing wind/dust exposure.

Basic rumen health, feed bunk management, avoiding sub-acute rumen acidosis and the addition of ionophores to the ration will decrease the number of gram positive bacteria in the rumen population that convert L-Tryptophan to 3-MI.

Since the metabolism of 3-MI produces free radicals that may contribute to lung damage, the addition of antioxidants like Vit E, Se to the feed (or even parenteral) may theoretically be beneficial.

As conclusion, AIP remains a prevalent disease in the feedlot industry, which evokes as many questions as answers. Treatment should either be emergency slaughter or treatment according to the normal BRD regimen (although unfavorable outcomes can be expected) and as prevention, attention should be given to decrease dust and digestive disturbances/abrupt dietary changes.