Y67-3Mimeo Report VY67-3
George T. Edds, D.V.M., Ph.D.
Chairman, Department of Veterinary Science
University of Florida
Aspergillus flavus, a mould frequently found on corn, peanuts,
rice, wheat or barley, produces a series of metabolites or compounds,
associated with toxicity from such mouldy feeds.1
Mol. Wt. 312
Mol. Wt. 328
In addition to its acute toxicity, aflatoxin B is an exceed-
ingly potent chemical carcinogen in rats,2 trout,3 aucklings,4 and
dogs. Aflatoxin B1 has an LD50 to ducklings 20 mg; G1 of 90
mg./kg.6 One mg./kg. of B1 in dogs produced death in 2-7 days with
severe liver damage. Chronic toxicity studies are characterized by
bile duct proliferation and carcinogenesis; ration contained 15%
peanut meal and the feed 7-8 ppm aflatoxin.
1. Anorexia, stunting or slow rate of growth, reduced feed
2. Some icterus and anorexia.
*Presented at the 10th Annual Veterinary Conference
Gainesville, Florida UME.
AUG 4 1972
3. "Hepatitis X syndrome" in dogs.
4. Tachypnea, fast-shallow breathing.
5. Delayed clotting time.
1. Icterus of mucous and serious membranes; pale, yellow liver.
2. Moderate to severe congestion of the liver, heart, lungs.
3. Edema and emphysema of the lungs.
4. Carcinoma of liver, lungs with spread to momentum and
5. Occasional hemorrhage into the gastro-intestinal tract.
6. Histopathologically, "bile duct hyperplasia."
1. Continued sampling of feed from Florida and Costa Rica to
determine levels and range of aflatoxin present.
2. Feeding of such potentially toxic feed to Hampshire chicks,
ducklings, mice, swine, and cattle with assays of meat or milk
for aflatoxin content.*
*Brown and Abrams, 1965, have reported:
1. Powdered milk, prepared from milk of the cows on toxic
rations as mentioned above, was extracted with methanol and
chloroform as described by de long, Vles and van Pelt (1964).
The dry and powdered extract so obtained was fed to ducklings
for four days without producing any visible histological
lesions or any of the biochemical disturbances noted earlier.
Thin layer chromatograms performed on this concentrated
preparation revealed no sign of aflatoxin or its metabolites.
2. A group of hens was maintained on a ration with an
aflatoxin content of 0.5 ppm for six weeks. After this
period eggs were collected from these hens and fed to a
further group of test ducklings, each bird receiving two
eggs per day for a period of eight weeks. During the same
period a similar group of ducklings received two eggs daily
obtained from hens maintained on a groundnut cake-free ration.
Besides the eggs, both groups of ducklings were given the
standard groundnut cake-free mashes used throughout this work.
3. Muscle tissue taken from ducklings with biochemically
and histopathologically confirmed chronic aflatoxicosis
was finely minced and dried in air in a dark room over-
night. Ten per cent of the duckling meat was included in
a groundnut-free mash fed to New Hampshire chickens. In
addition to this mash the dried minced meat was freely
available to the test chickens throughout the experiment.
Control birds were maintained on the standard groundnut-
free mash. The same procedure regarding slaughter and
examination of test and control birds was adopted. At
no time were any significant differences between test
and control birds observed.
Current Research: (continued)
3. Determine storage time and conditions permissible in mixed
feed on farms before significant levels of mycotoxins develop.
4. Determine whether addition of fungistats at time of feed
manufacture can prevent the development of toxic levels.
From the results of tests to date, it has been suggested that the
primary site of action is an interference in the metabolic systems
located in the mitochondria, especially the dehydrogenases. The
anemia may result from depressed protein synthesis, with the essential
disturbance being a markedly reduced rate or failure in ATP synthesis.
1Allcraft, R. and Carnaghan, R. B. A. Chem. Ind. London. 50, (1963).
2Barnes, J. M. and Butler, W. H. Nature.
3Ashley, L. M., Halver, J. E., and Wogan, G. N. Federation Procs.
23, 105 (1964).
4Butler, W. H. J. Path. Bact. 88, 189-195, (1964).
5Newberne, P. M., Russo, R., and Wogan, G. N. Path. Vet. 3, 331-340,
6Nesbitt, B. F., O'Kelly, J., Sargeant, K., and Sheridan, A. Nature
192, 1096, (1962).
7Brown, J. M. M., and Abrams, L. Onderstepoort J. Vet. Res. 32,