The passage of undigested feed in the faeces of broilers, shortened to feed passage is reported to be an improvement compared to earlier years.
During 1996 when global reports of feed passage occurred following consecutive years of poor grain harvests.
At that time, broilers were passing undigested feed in the faeces, evidenced by the presence of large corn particles, excess moisture, a characteristic green colouration with orange mucus, and poor formation of the faeces.
Affected broilers had poor pigmentation, poor feed conversion, and lower body weights, and flock uniformity was variable. On necropsy, lesions were commonly found in the proventriculus and gizzard of affected broilers.
Lesions were also found in the small intestines. It was interesting to note that in countries such as Guyana where alternative grains such as rice were fed, this syndrome did not occur.
According to recent reports, feed passage in broilers is occurring in individual farms or, in some cases, in entire integrations. The disease is not being observed on a global basis as in the past.
The tendency for broiler managers, from past experiences, is to immediately blame the feed quality. However, the lack of consistency of the problem in farms suggests other factors may need to be considered.
Following is a summary of factors that should be considered when the passage of undigested feed is noted in broilers. This summary is by no means complete, as additional etiologies will continue to be identified and added to the list. Feed passage syndrome in broilers, for purposes of this paper, will be defined as “the passage of nutrients in faeces due to improper digestion and/or absorption in the intestines.”
Clearly, the diseases described above are much different than the classical feed passage syndrome and include diarrhoea as only a part of their clinical expression. This information was presented simply to suggest that feed passage is a general term and is not associated with a specific disease syndrome, but occurs during many diseases. Feed passage results from some abnormality in the digestion and absorption of nutrients, and although the causes may be numerous, the clinical expression in the broiler is simply fed passage.
Causes of Feed Passage Syndrome
When broilers are heat stressed, they increase the consumption of water in an effort to cool down. Much of this water will be voided in the faeces, resulting in wet and poorly formed faeces.
Following heat stress, physical changes in the intestinal lining can be detected by histologic study within 48 hours and can be observed for at least 3 days. Changes include a decrease in villus length and surface area.
Dietary Salt Intake
When salt consumption is increased, broilers will consume additional water to assist in the elimination of the salt. This will result in broilers voiding much of the excess water by way of the faeces. The result is wet and poorly formed faeces. Excess salt intake can result from mixing errors in the feed, not taking into consideration the salt levels in some ingredients such as fishmeal when formulating, or not considering the salt levels in the drinking water
Damage to the lining of the intestine from clinical and subclinical coccidiosis can cause the passage of undigested nutrients in the faeces, especially in younger broilers. Feed passage is usually associated with the species, E. acervulina and E. maxima.
A coccidiosis monitoring program combined with an effective coccidiostat control program are recommended to ensure coccidiosis is not damaging the lining of the intestine and affecting the broiler’s ability to absorb nutrients.
Ascarids and Cestodes
Intestinal parasites can irritate the gut and cause passage of undigested feed in the faeces. A mild infestation of ascarids is enough to cause irritation and feed passage, while a significant cestode infection must occur before losses are recognized.
A number of viruses are associated with broiler feed passage. These include reovirus, calicivirus, adenovirus, parvovirus, enterovirus, coronavirus, togavirus, and others. Historically, reovirus has been considered a primary viral cause of broiler feed passage or “malabsorption syndrome.” However, it is now clear that this virus does not play a significant role in feed passage in broilers. Some investigators have described this virus as “one in search of a disease” as it is wrongly blamed for many syndromes in poultry. Reovirus infection is responsible for the disease of viral arthritis and vaccination to control this disease is recommended.
Bacterial enteritis often occurs secondary to viral or coccidial infections. Prevention is best achieved with effective use of growth promoters, control of coccidial infections, protection of immune system integrity, and comprehensive biosecurity and sanitation practices. The intestinal tract houses a large bacterial population that is necessary for its normal function. An imbalance in this flora can result in disease.
A specific bacterial infection in the gut that is increasing in incidence in recent years is necrotic Enteritis, caused by C. perfringens. This bacterium is common in the environment and is considered part of the normal gut flora of poultry. However, a disease associated with this bacterium is occurring with increasing frequency in recent years. A number of predisposing factors are recognized, including
- Damage to the gut from coccidiosis,
- Exposure to extremely high levels of the organism in the poultry house environment, dietary changes including pH and viscosity,
- High energy diets,
- Restricted feeding programs,
- Overstocking or high density,
- Saturation of the litter or poor litter management,
- Changes in the physical form of the feed (mash to pellets) during the grow-out, and feeding of some animal proteins.
More than 200 feed-related mycotoxins have been identified. Common examples include Ochratoxin A, which causes increased intestinal fragility and decreased shear strength. Aflatoxin causes liver damage, blockage of bile ducts, and decreased level of bile in the lower intestine. Poor fat absorption would result.
Trichothecene (T-2) is associated with lesions in the oral cavity, proventriculus, gizzard, and intestines. This mycotoxin is very caustic and causes chemical burns to the sites that it contacts.
Contamination sources for mycotoxins include mouldy grain, dirty feed bins, and contaminated feed transfer equipment. It is important to prevent the growth of mould in feed by purchasing only quality grains and storing grains under suitable conditions.
Inhibitors can be added to grains to restrict the growth of moulds. However, grains with higher levels of mycotoxins should have binding agents added and be blended with better quality grains to reduce negative effects.
Toxic levels of tannins in the feed cause esophageal and gastric edema, hemorrhagic ulceration, necrosis and sloughing of the mucosal lining, hypersecretion of mucin, and crop wall thickening.
This damage results in feed passage. Tannic acid is found in the coatings of grains, especially some varieties of sorghum. The presence of tannin in grains is of benefit to grain farmers in that higher levels will reduce consumption of the grains by wild birds during production in the field.
These compounds are present in low levels in animals, plants, and microorganisms. At higher concentrations they are toxic. Biogenic amines cause more problems in hot seasons when there is increased bacterial degradation of free amino acids, dietary proteins, and animal by-products.
Lesions associated with feeding toxic levels of biogenic amines include proventricular enlargement, gizzard erosion, sloughing of intestinal epithelia, poor weight gain and feed conversion, impaired immune response, and diarrhea. Affected birds are poorly pigmented and have low body weights and feed conversions.
This toxin is produced in over-processed fishmeal. It has an effect similar to the biogenic amine, histamine, in causing overproduction of hydrochloric acid in the proventriculus and resulting gizzard erosion. Toxicity is prevented through feeding only quality, properly processed fishmeal.
Feeding rancid fats to broilers is a common cause of feed passage, especially in hotter climates where fats readily become rancid if not stored properly. Lesions include proventriculitis, gizzard erosions, and enteritis.
The process involves the oxidizing of dietary ingredient fat and fat-soluble compound to produce free radicals or reactive oxygen molecules. Examples include the surperoxide radical (O2), hydrogen peroxide (H2O2), and hydroxyl radical (HO-). These compounds cause impaired immunity, poor growth, poor feed conversion, poor pigmentation, and gizzard erosion.
The composition of a broiler’s body is 60% water. It is essential that broilers drink adequate quantities of water in order to meet body demands. In many integrations, ensuring water quality is not considered a priority and consumption of poor quality water causes irritation of the gut and inefficient nutrient absorption leading to rapid feed passage.
Litter is the first material that recently placed chicks might consume, before finding feed and water. Therefore it is important to ensure litter is high quality, free from foreign materials, and fresh.
If quality litter is not available for the new flock, at least provide quality litter in the brooding area during the first week. Ingestion of contaminated litter can cause irritation of the gut linings of the young chick, resulting in poor nutrient absorption.
Feed passage in poultry will continue to be an occasional problem in poultry integrations. It is important to keep an open mind, as many factors need to be considered when investigating the problem.