Preventing Meat Production Loss from Coccidiosis

Summary

Background

Meat is a highly consumed American commodity.  The average US citizen consumes 67 pounds of beef per year [1] and 92 pounds of chicken[2].  Coccidiosis is an intestinal disease caused by bacteria[3]. Coccidia is common in livestock and causes loss of appetite, fatigue, dehydration and diarrhea.  It is considered a significant disease calves and chickens that can result in fatality[4].  Due to increasing demand for poultry and red meat, ranchers looked to prevent meat production loss from coccidiosis. The first coccidiostat, Sulfaquinoxaline, was produced in 1965. Coccidiostats are used to treat coccidiosis once symptoms are already showing[5].  Anticoccidants, on the other hand, stop the bacteria responsible for coccidiosis before the disease has infected the livestock.  Ionophores were the first anticoccidants. They were produced in the early 1970s then approved by the FDA 1975.  The European Union banned antibiotics for the use of growth promotion in 2006.  While ionophores are technically a class of antibiotics, they were not included in the ban due to their effectiveness as an anticoccidant[6].  Ionophores are still used as anticoccidants.  Concerns are raised as levels of popular commercial ionophores have been found in water and soil surrounding farmlands.

Figure 1: Data obtained from United States Department of Agriculture

The most common ionophores are monensin, salinomycin, lasalocid, tetronasin, lysocellin, narasin, and laidlomycin.   They can be produced biologically by microorganisms for intracellular ion transport[7].  Ionophores can be produced synthetically, however, the biological ionophores are used as anticoccidants.  Ionophores are considered nontherapeutic antibiotics.  They disrupt the ion concentration gradient causing ruminant bacteria to enter a futile ion cycle making them unable to maintain an effective metabolism [8].  The gram negative bacteria that the ionophores eliminate are responsible for inefficient feed digestion causing body weight gain to remain steady while food intake decreases [9].   These bacteria are also response for coccidiosis making the ionophores useful anticoccidants.

Ionophores disrupt the ion concentration gradient in two modes of action.  The carrier ionophore mode of transportation is shown in figure 2 (a).  The carrier ion shields the charge of that particular ion making it easier to pass through the hydrophobic membrane[10]. Channel forming ionophores, shown in figure 2 (b), create a hydrophilic pore within the membrane. This allows ions to pass through without interacting with the membrane[11].

Ionophores are deemed to be emerging environmental contaminants due to their heavy use in poultry and livestock production for the last 55 years[12].  Ionophores have relatively low amounts of studies on occurrence, fate and toxicological effects. The purpose of this paper is to outline the potential hazard, to characterize that hazard and identify possible courses of remediation for the past and future use of ionophores.

Hazard Identification

Ionophores are fed to the livestock and then can either remain in the animals’ tissues or are defecated in the form of the parent compound and its metabolites.  Studies to chicks have shown that even when treated with a large amount of ionophore the tissue concentration is low[13].   At zero time withdrawal from poultry, monensin has been reported at levels of 4.6 ug/kg in the liver and 2.0 ug/kg in muscle[14].  After one day of freezer storage, levels of monensin in kidney, liver, skeletal muscle and cardiac muscle were found to be 7.0, 7.5, 2.25 and 3.95 mg/kg [15].  The level of monensin was recorded at 1.46 mg/kg after 80 days of being frozen in the liver. Several studies have found that there is passage of monensin from the chicken to the egg[16]–[18].  The monensin in the egg has been found to decrease rapidly and considered negligible when the egg reaches the consumer[19]. Salinomycin was found to degradate within a number of days in chicken tissue[20]. There is an absence of studies of the pervasiveness of ionophores in cow tissue and if the acute amount in chicken tissue effects the other animals eating the meat.  Ionophores have been in heavy usage since their onset so it is unlikely that the amounts remaining in chicken and cows are toxic.  That does not rule out that there could be acute effects associated with these ionophores to the people who eat them.

Ionophores in livestock diet are not completely metabolized before leaving the body through defecation.  Figure 3 shows the amount of ionophores detected through the manure of various livestock animals’ feces.  Cows and sheep excrete 10% of Monensin as the parent compound[21]. Breakdown products are metabolized through demethylation, decarboxylation and hydroxylation reactions[19].  There are over 50 metabolites with no single metabolite prevailing.  The biological activity of the metabolites is considered less than the parent compound[19].   The ionophores that are not metabolized or remain in the tissue are defecated.