IMPROVED MILBOND-TX® “AFLATOXIN AND LIVER FLUKES IN DAIRY CALVES”
The liver must be maintained in a healthy state at all times because of the hundreds of vital roles it continuously plays each second in keeping the body healthy and functioning properly. Everything in an animal’s diet that is consumed digested and absorbed will eventually pass through the liver. This is also true for ingested toxins and many parasites. In fact, even though there are other routes for toxins and parasites to enter the body, the oral route is the most common. A major liver function, that all liver cells have, is related to clearing the body of toxins and many times, in so doing, the liver may be damaged by the same toxins and their metabolites it is filtering, detoxifying and excreting. Once parasites find a home in the liver they continue to cause problems which will, in most cases, if not treated lead to death of the animal. Once damaged by a parasite such as the liver fluke (Fasciola hepatica) or by a toxin such as aflatoxin (AFB1), any further insult to an already damaged liver will only make things worse. The worst-case-scenario would be for the liver to be forced to cope with AFB1 after it has already been infested with Fasciola hepatica (Fh). The negative additive effects of the worst-case-scenario, just mentioned,was first reported in a publication by Osuna et al., (1977).
Since their discovery, only 55 years ago, aflatoxins have been the most intensively studied mycotoxins in the world. The research published by Osuna and his coworkers was conducted only 15 years from the time of the discovery of aflatoxins and was at a time when research in this area of toxicology was still in its infancy. Once it was discovered in 1961 that the mold responsible for producing aflatoxins was from the Genus Aspergillus, especially Aspergillus flavus and Aspergillus parasiticus, awareness about the detrimental effects that aflatoxins caused in animals increased rapidly throughout the world. Most of the early experiments regarding the influence that AFB1 had on animal performance, after it was learned that AFB1 was a hepatotoxin, used an experimental design that would explore the “dose response relationship” and “cause and effect” when AFB1 was added to animal diets. Simply, different concentrations of AFB1 would be fed and the effects in various animals would then be documented. However, the above research conducted by Osuna and coworkers in the middle 1970’s was the first to show the synergistic effect that AFB1 would have in young ruminants known to be previously infected with Fh. This research was of extreme importance at the time, since for thousands of years it had been known that Fh had a devastating effect on liver function, but nothing in the middle 1970’s was known about the combined effect that the newly discovered AFB1, a known hepatotoxin, and Fh would have when both were present simultaneously in the animal.
EXPERIMENTAL TREATMENTS AND STUDY DESIGN
The entire experimental design and the complete in-depth results of this study, especially with regards to the blood components, can be found in the cited publication. However, the following is only a summary of the design and major results observed upon biopsy and necropsy in this study. Three oral doses of AFB1 (0.0, 0.5 and 1.0 mg/kg body weight) and 2 infection levels of Fh metacercariae (0 and 220) were used. (Note: metacercariae are the encysted resting or maturing stage of any trematode parasite and it is the infective stage of the trematode life cycle. Following ingestion, metacercariae hatch in the small intestine and migrate across the gut wall and to the liver where the juvenile flukes migrate through the liver tissue feeding and growing until they reach the bile ducts). Since young ruminants are more sensitive to AFB1 than yearlings and adults, four male Holstein dairy calves weighing an average of 45.8 kg each were allocated randomly to each of six treatment groups. The single oral dose of 220 metacercariae was given to all animals, except the control, at the initiation of the 10 week experiment and five weeks later the single oral dose of AFB1 was administered to all treatment groups except the control.
When compared to the control calves there were significant differences (P<0.05) in dry matter intake, body weight and serum albumin throughout the entire experimental period for treatment groups infected with metacercariae of Fh and AFB1. The decrease in dry matter intake in the AFB1 group of calves occurred immediately following the administration of the oral dose and the calves uninfected with metacercariae had a higher dry matter intake than infected calves. Once the oral dose of AFB1 was administered an immediate decrease in body weight was observed.
Compared to the calves receiving only metacercariae (Table 1) the single dose of 0.5 mg AFB1/kg body weight in the presence of metacercariae resulted in a definite increase in the number of Fh in the liver as well as an enlargement of the gallbladder. This observation was also apparent when the higher dose of AFB1 was administered to the calves. When the overall observations from biopsies or necropsies presented in Table 1 were considered, calves infected with metacercariae and administered the highest concentration of AFB1/kg body weight were the most seriously affected, thus, confirming the additive negative effects of AFB1 and Fh.
In studying toxicology it should never be forgotten that the concentration of dose and duration of exposure have a pronounced effect on the toxicity of any toxin. This research, using one acute dose of AFB1 in calves already infected with liver flukes contributed, at that time, to the “developing” base of knowledge about mycotoxins that had just been discovered 15 years earlier. These data collected in this publication and other data collected in the thousands of publications since this work was conducted has helped to understand the short and long term consequences of acute and chronic exposure to mycotoxins. Today, we know much more about AFB1 and other mycotoxins than in the mid-1970’s and today we also have inert clay-based feed additives, such as Improved Milbond-TX®, that are effective in binding AFB1. Of course, the best way to protect animals from the negative effects of AFB1 and other mycotoxins is to select and use feed ingredients in the diet that are of the highest quality.
Note: This issue of Milwhite’s Journal was compiled by Dr. Orlando Osuna and Dr. Richard Miles, Professor Emeritus, University of Florida, Gainesville, FL, USA.
Osuna, O, G.T. Edds and H.D. Blankespoor. 1977. Toxic effects of aflatoxin B1 in male Holstein calves with prior infection by flukes (Fasciola hepatica). Am. J. Vet. Res. Mar. 38(3) 341-349.
For additional information contact Dr. Orlando Osuna at 956-547-1970 or email@example.com.