Fog fever

Fog fever is a slightly confusing name. Affected animals don't have a high temperature, and the term 'fog' in the name actually refers to a second lush growth of grass, not misty or damp environmental conditions. The scientific name is Acute Bovine Pulmonary Edema (ABPE). The condition occurs in hungry, typically adult cattle, having been fed on dried feed indoors, and then moved to foggage pasture (fast growing, lush pasture, with high protein levels). The cattle graze on the new feed, clinical signs begin within 1 to 14 days and death often follows within 2 to 4 days after that. The condition can affect up to 50% of the herd, and around 30% of affected cattle may die as a result. A similar condition has been reported on a wide variety of grasses, alfalfa, rape, kale, and turnip tops.

Clinical signs

The bovine experiences difficulty breathing and will do everything it can to ease this discomfort. It will try to stand with its airway as straight and extended as possible, raising its head and stretching its neck forwards. Breathing rate will increase as high as 80 breaths per minute. there may also be extension of the tongue, and drooling. The animal may grunt as it breathes and froth may form around the mouth as the condition progresses. Rectal temperature will be normal, although some may show an elevated temperature from respiratory effort. ^[1]

Cause

'Fog fever' is a result of the biochemistry of the cattle stomach (rumen) being slow to adjust to a new diet. The cattle have been fed on a low-protein dried formulation indoors and the rumen is not prepared for the sudden exposure to high-protein grass. Specifically, the change in diet to lush vegetation rich in L-tryptophan causes a corresponding increase of the amino acid typically found in protein in the rumen; the level of L-tryptophan in crops is most likely to be high in lush, rapidly growing pastures, particularly (but not exclusively) in the fall. The bacteria in the rumen (specifically a Lactobacillus species) degrade L-tryptophan to indoleacetic acid, which can be converted to 3-methylindole (skatole) by some bacteria in the rumen, which is readily absorbed through the rumen wall into the portal circulation. (It is worth noting that 3-methylindole is produced exclusively from indoleacetic acid and not directly from L-tryptophan.) Club cells in the terminal bronchioles convert the 3-methylindole to 3-methyleneindolenine, which is toxic to the adjacent alveolar epithelial cells, leading to emphysema and pulmonary edema followed by death by asphyxiation.^[2]

Treatment

There is little that can be done for affected cattle. On no account should they be moved except on the advice of a veterinarian, since stress will kill many of the less severely affected.^[3]

Prevention

Ideally pastures should be used before they become overly lush and protein-rich. If this is not possible, the new diet should be introduced slowly by grazing the cattle just a few hours each day and increasing gradually, over a period of a fortnight. Cutting the pasture immediately before putting the cattle out may help. Drugs are available (monensin or lasalocid) which change the rumen biochemistry in preparation for high tryptophan levels, inhibiting the bacteria that convert L-tryptophan to 3-methylindole. Care must be taken to keep these products away from horses, for which, since horses have no rumen, they are toxic.^[4]

References