An acute form of interstitial pneumonia caused by L tryptophan is also known as fog fever, L tryptophan poisoning or Acute Bovine Pulmonary Emphysema and Oedema (ABPEO). Isolated cases of fog fever have been diagnosed in NZ but outbreaks in cattle have been reported in the Central Waikato region. Adult cattle and sheep are susceptible.
L tryptophan is an essential amino acid present in most proteins. Fog fever has been associated with the ingestion of lucerne, kale, turnip tops and rapidly growing pasture high in protein. An abrupt change from dry pasture to lush green pasture may trigger an outbreak of fog fever.
More than 4g/kg dry matter of 3MI in the feed may cause signs.
Rumen bacteria convert L tryptophan from the feed to 3 methylindole and indole. The 3 methylindole is absorbed into the blood and metabolically activated by the mixed function oxidase system in pulmonary epithelial cells to a pneumotoxic product that damages lung cells. Pulmonary oedema follows degeneration and necrosis of Type 1 alveolar cells in the acute phase. If the animal survives Type 2 alveolar proliferation occurs resulting in interstitial fibrosis. The initial toxicological event is probably the result of binding of 3 methylindole free radical covalently to cellular protein rather than lipid peroxidation. The plasma concentrations of 3 methylindole peak in 4 5 days and decline over 6 7 days. Indole does not cause pulmonary toxicity but is known to cause haemolysis.
Within 4 - 10 days of exposure to pasture or feed containing L tryptophan some cattle will die without any clinical signs. Other cattle may show sudden tachypnoea, expiratory dyspnoea, and an expiratory grunt. Cattle will breathe with open mouths, nostrils dilated, and head extended. Severely affected animals will not graze and if forced to move may collapse and die. The respiratory sounds during the early stages indicate consolidation. If the animal survives for several days sounds characteristic for interstitial emphysema are auscultated. Most severely affected animals die within 2 days after onset of signs. Survivors have harsh respiratory sounds and often develop chronic emphysema and are unthrifty.
The clinical signs for cows treated with indole (0.2 g/kg) are mild diarrhoea, haemoglobinuria, and haemolysis.
The lungs are bilaterally rubbery, wet, heavy and do not collapse when cut. In the early stages blood tinged, slightly viscous fluid is found in alveolar and interstitial spaces. The lungs may have white foamy exudate in the large airways. Patchy areas of emphysema and normal lung give the lung a marbled appearance. Petechiae and ecchymoses may be seen in laryngeal, tracheal and bronchial mucosa.
The metabolite indole does not cause pulmonary changes only histological lesions of haemoglobinuric nephrosis were found in indole treated cows.
A history of exposure to turnip tops or other lush feed such as lucerne, kale or rapidly growing pasture (reports on ryegrass/clover) is supportive. Only adult cattle and sheep are affected. Nursing animals are not affected.
Analysis of tryptophan levels in the feed are diagnostic (2 - 4 g/kg of Dry Matter are considered high).
In the lung histological lesions of interstitial pneumonia with a history of exposure support the diagnosis.
Infectious pneumonia.
Early recognition and treatment of the toxicity is important. The treatment of L tryptophan poisoning is largely symptomatic and supportive. If the exposure to tryptophan is less than 5 days, remove the animals from the source or give alternate feed. If the animals have been grazing for more than 6 - 9 days removing animals is not likely to prevent new cases.
Research suggests that early aggressive treatment to increase glutathione tissue levels (e.g. cysteine, sulphate) will decrease the severity of the effects on pulmonary tissue.
Treatment is recommended in severe cases only. Treat severe pulmonary oedema by giving 0.4 - 1.0 mg/kg frusemide IV or IM every 12 hours while limiting the amount of drinking water. The use of non steroidal anti inflammatory drugs may be beneficial especially when administered as soon as clinical signs appear. Flunixin (2.2 mg/kg IV daily) at the onset of illness may help to alleviate the clinical signs. Corticosteroids have been used but the efficacy has been difficult to assess.
Good if diagnosed early.
To reduce or prevent the incidence of toxicity limit the exposure to feed or pasture high in L tryptophan and alter the microbial flora with monensin (200 mg/head/day) to decrease ruminal production of 3 methylindole.
Bennell, D.G. (1966). A Non infectious Respiratory Disease of Bovines. N Z vet J. 14:73.
Connor, HE, The Poisonous plants in New Zealand, 2nd ed.,1977, Government Publications Ltd., Wellington
Hammond, A. C. Carlson, J. R. Breeze, R. G. (1980). Indole toxicity in cattle. Veterinary Record. 107(15): 344 346.
Kubow, S. Bray, T. M. (1988). The effect of lung concentrations of glutathione and vitamin E on the pulmonary toxicity of 3 methylindole. Canadian Journal of Physiology & Pharmacology. 66(7): 863 867.
Merrill, J. C. Bray, T. M. (1983). The effect of dietary and sulfur compounds in alleviating 3 methylindole induced pulmonary toxicity in goats. Journal of Nutrition. 1983. 113(9):1725 1731.
Radostits, O.M. Blood D. C. and Gay C.C. (1994). In Veterinary Medicine, Specific Diseases of Uncertain Etiology Diseases characterized by respiratory tract involvement. Veterinary Medicine 8th edition. 1687 1691.
Wikse, S. E. Leathers, C. W. and Parish, S. M. (1987) Diseases of cattle that graze turnips. Compendium on Continuing Education for the Practicing Veterinarian. 9(3):F115 F117.
Surveillance 1994 21(2):24 Tryptophan Poisoning in Grazing Stock