Nutritional Diseases

• Nutritional disease, any of the nutrient-related diseases and conditions that cause illness
in animals. Nutritional diseases also include developmental abnormalities that can be
prevented by diet, hereditary metabolic disorders that respond to dietary treatment, the
interaction of foods and nutrients with drugs, food allergies and intolerances, and potential
hazards in the food supply.
• A balanced diet is extremely important for the good health of an animal. Any imbalance in
the diet might lead to excess or insufficient intake of certain nutrients. Insufficient intake
of a particular nutrient can lead to a deficiency disease.

Common Nutritional Deficiency in Poultry

Disease Etiology Clinical Signs Diagnosis Prevention and
Control
Pododermatitis. It is a disease of the footpads characterized by erosion, ulceration, abscess formation, and
fibrosis.
Wet and poorquality Lameness and Clinical signs and Provide a dry and
litter. swollen footpads. histological ammonia-free litter.
Biotin deficiency. examination of Feed restriction in
Obese birds. footpads. both male and
female breeding
stock.
Encephalomalacia. It is a disease affecting the brain of the chicks that are primarily deficient in vitamin E. it is
also known as “crazy chick disease”.
Vitamin E or Uncoordinated History of the Sufficient amount
selenium movement. flock, signs, and of antioxidant.
deficiency. Loss of balance. lesions supported Avoid rancid fat or
Errors at the feed Convulsions. by histopathology rancid animal
mill. and response to byproducts in the
Lack of antioxidant ration.
vitamin E
in the feed. Store feed in
supplementation
Rancid fat or rancid wellmaintained bins
animal by product in the drinking
for short periods.
in the feed. water.
Avoid grains with
Mycotoxins in the excessive molds and
feed levels. mycotoxins.
Prolonged or poor
feed storage.
Rickets. It is a bone disorder associated with inadequate mineralization or calcification of bones with commonly
occurs in young, growing birds.
Dietary deficiency Reluctant to move Signs, Feeding diets
in calcium or and eat. postmortem containing required
imbalance in Lameness. findings of birds, levels of calcium,
calcium, Soft pliable beaks soft, and rubbery phosphorus, and
phosphorus, or and rubbery leg bones, and vitamin D3. Use
vitamin D3. bones. analysis of the antioxidant. Avoid
Flattened ribcage
existing diet. feeding birds with
and beading of the
rancid or moldy
ribs. feeds.
Perosis. It is a deformity in the distal end of the tibio-tarsal bone leading to either outward or inward bending of
the leg. It is also known as Chondrodystrophy. Severe enlargement of the hock joint and twisting of the end of the
tibio-tarsal bone can cause the gastrocnemius tendon to slip from the condyle groove at the distal end of the
tibiotarsus. Thus, the condition is also called “slipped tendon”.
Feeding diet Reluctant to walk. Clinical signs and Adequate levels of
deficient in Difficulty reaching characteristic leg manganese, zinc,
manganese or an feed and water. deformity and calcium,
imbalance of Twisting or bending analysis of the phosphorous, iron,
calcium and of the tibia and existing diet. and all B-vitamins
phosphorus in the
metatarsal epiphyses ate present in the
diet.
in displacement of diet.
Partial or absolute
the Achilles tendon
deficiency in zinc,
or gastrocnemius
folic acid, choline,
tendon.
and biotin.
Nutritional Myopathy. It is also called muscular dystrophy or “white muscle disease” because of the presence of
light-colored streaks of bundles of muscle fibers in the breast and thigh. In severe cases, there is degeneration of
the gizzard and heart muscle.
Vitamin E and Depression and slow Necropsy findings Use stable forms of
selenium deficiency growth. are usually antioxidant in the
accompanied by a characteristics feeds.

sulfuric amino acid Lesions in skeletal and diagnostic of Avoid giving rancid
deficiency. muscles, gizzard, “white muscle feeds to the birds.
and heart muscles. disease” Selenium at dietary
levels of 0.04-0.1
ppm.
Exudative diathesis. It is a nutritional disorder characterized by the accumulation of fluid in the subcutaneous tissue
due to abnormal increase in blood capillary wall permeability.
Deficiency in Accumulation of a Presence of Stable forms of
vitamin E and greenish-blue fluid greenish-blue antioxidant in the
selenium. under the skin over viscous fluid that feeds.
the breast and leg is easily seen Avoid feeding of
areas. under the skin. rancid feeds to
Sudden death occurs chicks.
in severe cases. Concentration of
selenium of 0.040.1
ppm.
Curled Toe Paralysis. This due to riboflavin deficiency. Many tissues may be affected by riboflavin deficiency,
although the epithelium and the myelin sheaths of some of the main nerves are major targets. Changes in the sciatic
nerves produce “curled-toe” paralysis in growing chickens.
Riboflavin Reluctant to move . Histological Daily 100-mcg
deficiency. Leg muscles are examination of doses for chicks or
atrophied and the affected poults, followed by
flabby. nerves shows an adequate amount
Skin is dry and degenerative of riboflavin in feed.
harsh. changes in the
Chicks lie prostrate myelin sheaths
with their legs that, when severe,
extended. pinch the nerve.
Enlargement of the
sciatic and brachial
nerve sheaths.
Fatty liver hemorrhagic syndrome (FLHS). It is a metabolic condition that affects chickens worldwide. Sudden
death of birds in full production is the most common complaint. Key findings are excessive fat in the liver,
associated with varying degrees of hemorrhage.
Associated with Liver is usually Fatty liver Monitor body weight
high-energy diets enlarged, putty hemorrhagic and daily feed
and restricted colored, and friable. syndrome is easy intake. Substitute
exercise. Abdominal cavity to recognize at supplemental fat for
often contains large necropsy because carbohydrate, while
amounts of oily, of the liver keeping total energy
unsaturated fat. hemorrhage and stable.
Ovary is usually because the liver On farms with a
active. is enlarged and history of FLHS,
Affected birds often engorged with fat. diets should include
have pale combs. at least 0.3 ppm
selenium.

Common Nutritional Deficiency in Swine

Protein deficiency, which may result from suboptimal feed intake or a deficiency of one or more of the essential
amino acids, causes reduced gains, poor feed conversion, and fatter carcasses in growing and finishing pigs. In
lactating sows, milk production is reduced, excess weight loss occurs, and sows may fail to exhibit postweaning
estrus or have delayed return to estrus. For optimal use of protein, all essential amino acids must be liberated during
digestion at rates commensurate with needs. Therefore, protein supplements should not be handfed at infrequent
intervals but should be mixed with the grain or be available at all times with grain on a free-choice basis. No
evidence has been presented to support the theory of “protein poisoning” in pigs. Diets containing as much as 35%–
50% protein were found to be laxative and less efficiently used, but no toxic effects were noted.
Fat deficiency. Certain long-chain polyunsaturated fatty acids are essential for swine. Linoleic acid is essential in
the diet and is used to produce longer-chain fatty acids that are probably also essential. A linoleic acid deficiency
induces hair loss, scaly dermatitis, skin necrosis on the neck and shoulders, and an unthrifty appearance in growing
pigs. Conventional swine diets generally contain adequate fat from the natural ingredients to furnish ample amounts
of essential fatty acids.
Deficiencies of calcium or phosphorus result in rickets in growing pigs and osteomalacia in mature pigs. Signs
include deformity and bending of long bones and lameness in young pigs, and fractures and posterior paralysis (a
result of fractures in the lumbar region) in older pigs. Sows that produce high levels of milk and nurse large litters
are particularly susceptible to posterior paralysis toward the end of lactation or after weaning if dietary calcium or
phosphorus is deficient. These signs can also result from a deficiency of vitamin D, but phosphorus deficiency is
the most common cause.
Pigs fed diets low in salt (NaCl) grow poorly and inefficiently, largely because of a marked reduction in feed
intake. Although not specific for salt deficiency, poor hair and skin condition may also develop. There have been
reports of salt-deficient pigs attempting to consume urine of other pigs.
Sows fed diets deficient in iodine produce hairless pigs that are weak or stillborn. With a borderline deficiency, the
newborn pigs may be weak only at birth, but their thyroids are enlarged and have histologic abnormalities.

Some feedstuffs (including soybeans and soybean meal) contain goitrogens that may cause marginal goiter if iodine
is not included in the diet. Iodized salt at recommended levels prevents this deficiency.
Deficiencies of iron and copper reduce the rate of Hgb formation and produce typical nutritional anemia. Signs
of nutritional anemia in suckling pigs include low Hgb and RBC count, pale mucous membranes, enlarged heart,
skin edema about the neck and shoulders, listlessness, and spastic breathing (thumps). Iron deficiency is more
common than copper deficiency and is most common in nursing pigs that do not receive an iron injection or oral
iron early in life.
A deficiency of zinc results in parakeratosis in growing pigs, particularly when fed diets high in phytic acid (or
phytate, the primary form of phosphorus in cereal grains and oilseed meals) and more than the recommended
amount of calcium. The exact mode of action of zinc in the prevention of parakeratosis is not known.
Deficiencies of selenium and/or vitamin E can cause sudden death of young, rapidly growing pigs. In addition,
selenium/vitamin E deficiency in nursing pigs makes them more susceptible to iron toxicosis from iron injections.

Most commercial diets are fortified with vitamins, and vitamin premixes are readily available for farm-mixed feeds,
so deficiencies are less common than they were years ago. Deficiency of vitamin A results in disturbances of the
eyes and the epithelial tissues of the respiratory, reproductive, nervous, urinary, and digestive systems.
Reproduction is impaired in sows, and they may farrow blind, eyeless, weak, or malformed pigs. Herniation of the
spinal cord in fetal pigs is reported as a unique sign of vitamin A deficiency in pregnant sows. Growing pigs
deficient in vitamin A show incoordination and develop night blindness and respiratory disorders. Vitamin A
deficiency is rare because of the ability of the liver to store this vitamin.
Signs of vitamin D deficiency include rickets, stiffness, weak and bent bones, and posterior paralysis. These signs
are indistinguishable from those of a calcium or phosphorus deficiency
Vitamin E deficiency can result in poor reproduction and impaired immune system. Many of the signs of vitamin
E deficiency are similar to those of selenium deficiency.
Pigs deficient in vitamin K have prolonged blood clotting time and may die from hemorrhages. Certain
components in moldy feed can interfere with vitamin K synthesis. Also, excessive levels of dietary calcium interfere
with vitamin K activity, causing these signs.
In pigs deficient in riboflavin, reproduction is impaired; post-pubertal gilts fail to cycle but show no other clinical
signs. Deficient sows are anorectic and farrow dead pigs 4–16 days prematurely. The stillborn pigs have very little
hair, often are partially resorbed, and may have enlarged forelegs. Growing pigs fed diets low in riboflavin gain
weight slowly and have a poor appetite, a rough coat, an exudate on the skin, and possibly cataracts.

Pigs deficient in niacin have inflammatory lesions of the digestive tract and exhibit diarrhea, weight loss, rough
skin and coat, and dermatitis on the ears. Intestinal conditions can be due to niacin deficiency or bacterial infection.
Deficient pigs respond readily to niacin therapy and, although not a cure for infectious enteritis, adequate dietary
niacin probably allows the pig to maintain its resistance to bacterial invasion.
Growing pigs and pregnant sows develop a typical “goose-stepping” gait, ataxia, and a noninfectious bloody
diarrhea when maintained on diets deficient in pantothenic acid. When the deficiency becomes severe, anorexia
develops.
Pigs with a choline deficiency exhibit incoordination and an abnormal shoulder conformation. At necropsy, they
may have fatty livers and usually show kidney damage. Sows deficient in choline have reduced litter size and may
give birth to spraddle-legged pigs.
Biotin deficiency includes excessive hair loss, skin ulcerations and dermatitis, exudates around the eyes,
inflammation of the mucous membranes of the mouth, transverse cracking of the hooves, and cracking or bleeding
of the footpads.
Neonatal pigs fed synthetic diets low in vitamin B12 show hyperirritability, voice failure, and pain and
incoordination in the hindquarters. Histologic examination of the bone marrow reveals an impaired hematopoietic
system. Fatty livers are also noted at necropsy.

Common Nutritional Deficiency in Cattle

 Sign Possible Nutrient or Dietary Involvement
Abortion Deficiencies of trace minerals or vitamins, especially selenium, vitamin A, or vitamin E

Anemia Possible copper or cobalt deficiency in adult cattle; iron deficiency in young calves
(unlikely in adult cattle)
Blindness and night May be an initial isolated sign of polioencephalomalacia; may be associated with vitamin
blindness A deficiency, with or without signs of corneal opacity
Bloat Consumption of legume pastures or finely ground, high-starch diets (such as are
frequently fed to feedlot cattle) are predisposing; cattle not acclimated to these diets are
particularly susceptible
CNS signs Incoordination, blindness, nystagmus, thrashing, and opisthotonos may be associated
with polioencephalomalacia; high-starch diets with microbial inactivation of thiamine
and high-sulfur diets such as those associated with heavy feeding of distiller’s grains and
solubles
Congenital defects Deficiencies of vitamin A, manganese, or copper
Convulsions Sign of vitamin A deficiency, particularly if they occur intermittently interspersed with
periods of normal activity in growing calves; should be differentiated from nervous
coccidiosis
Cystic ovaries Energy insufficiency and associated subclinical ketosis in early lactation are
predisposing; vitamin E and selenium deficiency speculated to contribute
Diarrhea Numerous dietary factors, including abrupt changes in diet, especially those associated
with increases in dietary nonfiber carbohydrates and dietary rumen fermentability; lush
rapidly growing pasture and increased dietary protein or salt concentrations
Displaced abomasum Both metabolic and nutritional causes; feeding should be to prevent ketosis and stimulate
high dry-matter intakes; both pre- and postpartum diets are important in management
Dyspnea Atypical interstitial pneumonia associated with movement of cattle from poor pasture to
lush pasture; associated with ruminal conversion of tryptophan to 3-methyl indole
Fatty liver Overfattening in late lactation or during the dry period accompanied by poor feed intake
in late gestation and early lactation
Hypomagnesemic Functional and absolute magnesium deficiency; risk increases with consumption of lush
tetany pasture grasses, especially with high potassium concentrations
Inappetence (off feed) Many nutritional deficiencies (protein, mineral, vitamin) eventually result in reduced feed
intake
Incoordination Blind staggers associated with chronic selenium intoxication;
demyelinization associated with copper deficiency
Infertility Energy is the most clearly associated nutrient; insufficiencies of carotene or manganese
may affect ovarian function
Ketosis Excessive lipid mobilization and insufficient gluconeogenesis; overfattening in late
gestation and insufficient feed intake in early lactation are the primary nutritional
influences
Laminitis Chronic or acute laminitis and their sequelae are thought to result from diets with high
concentrations of nonfiber carbohydrates
Milk fever (parturient Caused by failure of calcium homeostasis rather than dietary calcium deficiency; control
paresis by feeding low-calcium diets or acidifying diets prepartum
Pica and dirt eating Common causes are not well determined; sodium deficiency, potentially phosphorus
deficiency, low-fiber diets implicated
Polioencephalomalacia Associated with either ruminal destruction of thiamine or with ruminal production of
hydrogen sulfide associated with high-sulfur diets; more common in feedlot than dairy
cattle
Retained fetal Deficiencies of selenium, vitamin A, or vitamin E, but adding these nutrients to adequate
membranes diets will not reduce incidence; metabolic problems associated with prepartum negative
energy balance may also be predisposing
Rickets and Insufficient calcium, phosphorus, or vitamin D consumption
osteomalacia
Rumen acidosis, acute Usually associated with major errors or inconsistencies in feed delivery in which high
clinical starch intake occurs in cattle unaccustomed to such diets; associated with formation of
lactic acid in the rumen with severe drops in rumen pH
Rumen acidosis, Associated with lactation diets with high nonfiber carbohydrate concentrations and low
chronic subclinical fiber concentrations; also associated with high rumen concentrations of volatile fatty
acids and rumen pH values ≤5.2
Skin problems Problems such as dull, brittle hair coats, hypotrichia, easily depilated hair,
hyperkeratosis, thin skin, and poor healing may be associated with nutritional problems;
deficiencies of vitamin A and zinc, generalized protein-calorie malnutrition
Sudden death Deficiencies of vitamins A or E, selenium, or copper
 Suppressed immunity Generalized immunosuppression, including both cellular and humoral immunity, may
occur due to malnutrition; specific nutrient deficiencies include vitamin A, vitamin E,
zinc, copper, and selenium; also generalized protein-calorie malnutrition
Toxicities Many toxicities associated with feedborne toxicants; including nitrates, cyanide, many
mycotoxins, toxic plants
Urolithiasis Diets with high phosphorus and low fiber concentrations
Wasting and failure to Signs of many nutritional deficiencies, as well as of chronic diseases such as internal
thrive parasitism; cobalt deficiency is a well-documented cause of ill thrift in cattle;
proteincalorie malnutrition should always be evaluated
White muscle disease Dietary deficiency of selenium or vitamin E

MYCOTOXINS IN FEEDS

Mycotoxins
• Fungal metabolites that can cause serious problems in the quality of agricultural
commodities
• Secondary metabolites with no biochemical significance in fungal growth and
development (Mass, 1991)
• Produced mostly by saprophytic fungi in post-harvest crops
• Some are produced by endophytic fungi during plant growth
• Generally lipophilic o Tend to accumulate in fat fraction of plants and animals
• Ruminants are more resistant to adverse effects of mycotoxins (Wogan, 1966; Helferich
et al., 1986)
• More than 300 different mycotoxins have been identified

Effects of Mycotoxins
• Feed ingredient o Can degrade nutrient
content of ingredients
• Mixed feeds o Can reduce palatability
of feeds o Can reduce feeding value of
fees
• Animal o Reduced feed efficiency o
Slow growth o Impaired reproduction o
Increased incidence of diseases
• Profit o Feed wastage o Reduced farm
productivity o Poor quality of products
o Reduced consumer acceptance of products
• Food safety o Risk to human health
(WHO-IARC, 1993)
Aflatoxins are carcinogenic to human

Aflatoxins
• Produced by Aspergillus flavus, A. parasiticus, and A. niminus
• Named aflatoxin in 1960 after discovering that the cause of turkey “X” disease was A.
flavus toxins.
• Preferentially grow under hot and humid conditions with an optimal temperature of
2533°C
• Corn, peanuts, and cottonseeds are crops that are most commonly affected by A. spp.
• Drought, insect infestation, and poor storage conditions can increase occurrence
• Most widely studied mycotoxins (>5000 publication) o Widespread distribution o Potent
toxicity
o Potential carcinogen in human
 Aflatoxin B1, followed by G1, B2, and G2
Aflatoxin M1 – less carcinogenic but hydroxylated metabolites is excreted
in milk
• Primary target organ – liver
• Metabolites bind to proteins, DNA, and RNA
• Acute effects of aflatoxicosis o Reduced body weight gain o Depression of feed intake
o Liver damage

Ochratoxin (OTA)
• Metabolites of both Aspergillus and Fusarium species
• Known for nephrotoxic effects
• Causative agent of kidney disease in pig known as mycotoxin porcine nephropathy
• Grains, particularly barley, and oilseed crops are susceptible to OTA
• Can reduce weight gains and performance in swine (Cook et al., 1986) and poultry (Huff
et al., 1988)
• Other symptoms include diarrhea, increased water consumption, diuresis and dehydration
• Potential transmission into human food chain
• OTA exerts their toxic effect mainly on the kidney at levels of 0.20 to 4.0 ppm
• At higher levels (5-10 ppm), other organs such as the liver, intestine, spleen, lymphoid
tissue and leukocytes can be affected.

Citrinin
• Produced by Penicillium citrinum and P. verrucosum on cereal and oilseed crops • It
produces effects similar to those of OTA most notably nephropathy.
• Citrinin is at least 10 times less nephrotoxic than OTA (Rumbeiha, 2001)
• Citrinin and OTA often occur together as contaminants of feedstuffs

Trichothecenes
• Group of structurally related compounds of tetracyclic sesquiterpene structure
with a sixmembered oxygen containing ring • Mainly produced by Fusarium
species
• Toxic effects:
o Gastrointestinal disorders such as vomiting, diarrhea o Feed refusal
o Compromised growth o Abortion
o Anemia
• Deoxynivalenol (DON) or vomitoxin is produced by F. graminearum o Swine
are very sensitive to DON
A reduction in feed consumption and weight gain (at 2-3 ppm of purified
DON)
Poultry and ruminants can tolerate levels of 20 ppm DON o FDA
recommends that grains and grain by-products for animal feeds should not
contain >5 ppm DON
• T-2 toxin o Produced primarily by F. sporotrichioides and F. poae o In poultry:
Drastic and sudden decrease in egg production
Decreased shell quality
Abnormal feathering
Mouth lesions
Decreased weight gain

Zearalenone (ZEA)
• A resorcyclic acid lactone compound with estrogenic properties o Capable of binding to
estrogen receptors o Toxicity signs are evidenced by hypoestrogenism
• Produced by Fusarium species
• Swine appear to be most susceptible to ZEA (Diekman and Green, 1992) o Gilts:
 Reddening and swelling of the vulva
Increased size of the uterus
Mammary enlargement
Rectal and vaginal prolapse
o In boars:
Testis atrophy
Nipple enlargement
Rectal prolapse
o In sows:
Prolonged estrus
Ovarian atrophy
Pseudopregnancy
Abortion
Stillbirths
Birth of weak pigs
• Hyperestrogenism can be observed in immature gilts within 1
week of feeding ZEA at 1.5 to 2 ppm.
• Effects are reversible
• Usually disappear 1 to 2 weeks after withdrawal of ZEA – contaminated feeds
• Broiler chicks and laying hens – not susceptible to ZEA even at very high concentration
(Feedstuffs, 2002).

Fumonisin
• Group of compounds most commonly found in corn and corn by-products.
• Produced by F. verticilloides and F. proliferatum
• Structurally similar to sphingosine
• Liver – primary target organ in most species
• Lungs and pancreas are specific in swine o Fumonisins are associated with porcine
pulmonary edema syndrome and hepatic injury (Motelin et al., 1994).
• Poultry are apparently more resistant

Other Mycotoxins
• Patulin o Produced by Penicillium, Aspergillus and
Byssochlamys
o Most likely occur in moldy fruits such as apples but may also be found in grains
especially wet grains and silage.
o Patulin is antibiotic gram-positive bacteria o Potential toxicity in livestock is low
but there are reported case studies of toxicity.

• PR toxin o Produced by P. roquefortii

o Found in silage and suspected vector of symptoms of abortion and retained
placenta.
o Associated with silage toxicity

• Mycophenolic acid (MPA) o MPA has antifungal,

antibacterial and antiviral activities and is used for immune
system repression in organ transplant patients.
o Its toxicity to animals appears to be low. o Produce by number of fungal genera
but is of most concern because of production of Penicillium that occurs frequently
in silages.

Mode of Mycotoxin Action

• Aflatoxins o Carcinogenic and cytotoxic o Inhibit
DNA and RNA synthesis o Induce lipid peroxidation
(oxidative damage)
 o Inhibit cyclic nucleotide phosphodiesterase activity in brain, liver, heart and
kidney tissues
Regulate cellular levels of the second messenger, cAMP and cGMP cAMP
has many functions (i.e., regulation of carbohydrate and lipid metabolism)
• Ochratoxins o Contain portion structurally analogous
to mitochondrial enzyme active sites
Competitively binds substrates o Affects activities of ATPase, succinate
dehydrogenase, cytochrome C oxidase (cellular respiration)

• Trichothecenes o Inhibition of protein, DNA, RNA

syntheses o Disruption of membrane transport and
function o Suppression of immune response

• Zearalenone o Binds to estrogen

o Mimics the action of estrogen

• Fumonisins o Disrupts sphingolipids metabolism by

inhibiting sphingosine N-acetyltransferase o Also
inhibits arginosuccinate synthetase (urea cycle) and
protein phosphatases (protein metabolism)

• Mycotoxin Interaction o Mixture of multiple

ingredients
o Molds of the same genus can produce more than one mycotoxin o Interaction
between mycotoxins is complex o May be antagonistic, additive or synergistic in
nature o May vary depending on mycotoxins combination and level

Mycotoxin Combination Interaction

Aflatoxin and ochratoxin Synergistic

Aflatoxin and deacetoxyscirpenol (DAS) Synergistic

Aflatoxin and DON Additive

Aflatoxin and T-2 Synergistic

Ochratoxin and T-2 Synergistic

DON and fusaric acid Antagonistic

Source: The Mycotoxin Blue Book (2005) as cited by Martin and Sacranie, 2005.

Mycotoxins Control and Prevention

• Best approach to control mycotoxin:
o Prevent fungal growth
o Adequate drying, processing and good storage facilities
• Addition of feed additives such as mold inhibitors and mycotoxins adsorbents

Adsorbents Must Have the Following Characteristics (Martin and Sacranie, 2005)
• Capable of binding the broadest possible range of mycotoxins and with proven efficacy in
co-contamination.
• Does not bind dietary minerals or vitamins
• Can be used at a low, effective inclusion rate (<0.20%)
• Able to bind mycotoxins in the aqueous environment of the gut within 30-minutes of feed
ingestion, preventing uptake of the toxins into the bloodstream
 • Proven in-vivo, with research published in peer-reviewed scientific journals
• Demonstrates high affinity for mycotoxins when present in feed at low (ppm) levels

ANTI-NUTRITIONAL FACTORS

ANF
• Substances that inhibit normal absorption and utilization of nutrients present in feedstuffs
• Normal constituent of varying chemical composition like proteins, carbohydrates and fatty
acids
• Processes such as washing, soaking and heating can inactivates ANFs

Protease Inhibitors (Trypsin inhibitor)

• All legumes contain protease inhibitor
• Inhibit trypsin and chymotrypsin – lowers protein digestion
• When trypsin or chymotrypsin attempts to digest trypsin-inhibitor protein, the inhibitor
binds irreversibly to the enzyme.
• Can be destroyed by heat treatment
• Most common assay used to estimate protease inhibitor content is the urease activity.

Gizzerosine
• Dipeptide that has been identified as the causative agent of toxicosis known as the “black
vomit” in broiler chickens.
• Contents of the esophagus and crop turns black due to the presence of acid-digested blood
from the gizzard.
• Formed during over dry heating of fishmeal
• Potent stimulator of histamine, which causes excessive gastric acid secretion (HCl) and as
severe reduction in pH at the proventriculus and gizzard
• Extremely low pH damages the submucosa layer of the gizzard leading to erosion,
ulceration and perforation.

Lectins
• Glycoproteins (60,000-100,000 MW) that have the ability to bind to
carbohydratecontaining molecules.
• Bind to the sugar moiety of the surface membrane of gut wall.
o Severe disorganization and destruction of the normal morphology of the regularly
folded structure of microvillus membrane
• Cause damage to the microvilli in small intestine – impaired nutrient absorption
• Soybean lectins accounts for 25% of the growth inhibition produced by raw soybeans

Mimosine
• An aminopropionic acid, found in ipil-ipil o In pigs, causes alopecia (5% max allowed) o
In layers, causes molting (5% max)
• Toxicity causes alopecia, dermatitis, lesion in esophagus, and poor growth
• In ruminants, mimosine is metabolized in the rumen to a metabolite, dihydropyridone that
is goitrogenic causing animals grazing Leucaena to develop enlarged thyroid glands
(Cheeke, 1999).
o Dihydropyridone – interferes with iodine uptake

Non-Starch Polysaccharides (NSP)

• Structural carbohydrates present in endosperm cell wall of cereal grains
• Insoluble NSP – cellulose (indigestible)
 • Soluble NSP – i.e., arabinoxylans, beta-glucans, mannans o Increase the viscosity of
ingesta in the gut
o Hinders effective interaction of digestive enzymes and substrates at the mucosal surface.
o Efficiency of nutrient absorption through the intestinal wall is reduced
• Soluble NSP possess high water absorbing capacity o Increases the ingesta volume
once inside the gut, restricting feed intake.
Phytic Acid
• Bound form of phosphorus in plant sources
• Only 20-40% of the P in plants are utilized by the animals o Due to lack of enzyme phytase
in monogastric animals
• Binds minerals/metal ions, therefore affecting absorption of Ca, P, Zn and other minerals
• Phytic acid in the form of phytate causes poor utilization of phosphorus, calcium, other
minerals, protein and energy in pigs and poultry (Finnfeeds, 2003)

Tannins
• Phenolic compounds that can bind proteins and carbohydrates
• Highest content in sorghum (2.7 to 10.2%, Jasman, 1993)
• Present in testa and pericarp of sorghum (Cheeke, 1999)
• Darker sorghum – higher tannin content
• Lowers amino acid bioavailability
• Form complexes with protein that resists digestion
• Means to control the adverse effects of dietary tannins include dietary supplementation of
dl-methionine and addition of tannin-binding agents like gelatin, polyvinylpyrrolidone and
polyethylene glycol (Cheeke, 1999; Leeson and Summers, 20021)

Saponins
• Large group of structurally related substances with properties resembling those of soaps
and detergent
• 2 groups of saponins; triterpenoid aglycone and steroidal aglycone
• Saponins found in grains are of triterpenoid aglycone type
• Present in alfalfa, sunflower, lupins, chickpeas, soybeans, and peanuts
• Saponins have bitter taste, mucosal irritating properties, detergent (foam) properties and
have the ability to form complex with bile acids and cholesterol (Leeson and Summers,
2001).
o Hypocholesterolemic effect of garlic in humans due to saponin in garlic

Cyanogenic Glycosides
• Raw cassava has high cyanogenic glycosides
• Absorbed rapidly in the GIT and dissociates in the blood
• Free cyanide can block respiratory chain leading to death o Binds to cytochrome c oxidase
(4th complex in ETC) forming a stable complex and blocking the respiratory chain halting
ATP production. o Animal is deprived of chemical energy to perform many processes that
sustain life
• Mortality occurs only when the cyanogenic plants are offered fresh and unprocessed
(Leeson and Summers, 2001).
• Adequate processing of cassava is needed.

Philippine Feed Laws and Regulations

• RA 1556 (as amended by PD # 7) – Livestock and Poultry Feeds Act

• BAI Administrative order # 35 – Livestock and Poultry Feeds Regulations
• Republic Act No. 1556 o An act to regulate and control the manufacture, importation,
labelling, advertising and sale of livestock and poultry feeds.
o Enforcing official: Department of Agriculture – Bureau of Animal Industry
Provisions of the Philippine Livestock and Poultry Feed Regulations
• Registration o No feeds/feeding stuff in the form of complete mixture, concentrate,
supplement, or ingredient which have not been registered with the director (BAI) shall be
manufactured, imported, advertised, sold or offered for sale, or held in possession for sale
in the Philippines.
o No change in the brand of a registered feed of feeding stuff shall be made without
a written notification to the director.
o No commercial feeds/feeding stuff shall be registered
If the brand thereof is identical or will likely be confused with another brand
already applied to a registered feeding stuff;
If the specific name of each and every ingredient of mixture, base or
concentrates, and supplement is not clearly stated; or
If the feeds or feeding stuffs do not conform to the provisions of this act.
• Labeling o All feed and feed ingredients should have complete label with guaranteed
analysis.
o The net weight in metric equivalent of the contents.
Not gross weight of feed and container
10, 25, 40, 50 kg/pack
o The name, brand or trademark and nutritive purposes. o The name, and principal
address of the manufacturer or person responsible for placing the commodity on
the market. o The minimum percent of crude protein.
o The minimum percent of crude fat. o The maximum percent of crude fiber.
o The maximum percent of ash. o The maximum percent of moisture. o In the case
of mixed feeds containing more than five (5) percent of mineral ingredients, the
maximum percentage of calcium (Ca) or phosphorus (P). o In the case of feeds or
feeding stuffs intended to be used as feed supplements or premixes for which
special qualities are claimed, such as vitamin, mineral, arsenical, surfactant,
unidentified growth factor, hormone, antibiotics, and amino acid contents, a
definite guarantee relative to its quality.
o Feeds containing drug or drug ingredients for the prevention of diseases of livestock
should be labeled to show:
The name and percentage of drug used
Directions for use
Warning against use under those conditions in which its use may be
dangerous to the health of livestock and man
Misleading advertisement – labels of containers of feed and/or feeding stuff
must not contain any form of advertisement and/or claims that are false and
misleading. Any advertisement containing any claim that the feeds is suited
for all purposes shall considered a misleading advertisement under this
order.
The use of urea in mixing feeds or the sale of mixed feeds, feedstuffs and
ingredients, containing urea is prohibited except for mixed feeds for
ruminants, the amount in which should appear in the label.
Labels of local grains and/or their by-products, minerals and other
ingredients sold or to be sold for feed shall show conspicuously and clearly:
Net weight
Name of feed (e.g., rice bran, yellow corn, white corn, ipil-ipil, copra,
shell powder, rice hay, etc.)
Conditions (e.g., whole grain, cracked, middling’s, ground, fine or
coarse, etc.)
Class (e.g., second or third, as prescribed by standards set by the
director)
Name and address of store
Registration number of store owner
Quality Control Service
• Section 9. All person engaged or desiring to engage in the manufacture of mixed feeds for
commercial purposes, shall establish and maintain a quality control laboratory and shall
retain the services of licensed chemist and a veterinarian or a licensed chemist and an
animal nutritionist to be responsible for the analysis and test of mixed feeds before they
are released for sale to determine their conformity with the feed formula of the particular
feed and feeding stuff. o Animal nutritionist
Has at least a scholastic credit of nine (9) units in animal nutrition for a duly
recognized educational institution and five (5) years’ experiences in
compounding animal feeds in a duly registered feed mill.
One who has a degree in animal science major in animal nutrition.
• Section 10. It shall be mandatory to all persons engaged in the manufacture of feeds for
poultry and swine for commercial purposes to maintain livestock to be fed with its
manufactured feeds for experimental purposes.
o Animals not less than:
Poultry – 50 for broilers, 50-day-old pullets, 50 growers, and 50 layers
swine – 5 piglets, 5 growers, 5 breeding gilts and sows and 5 finishers
o Provided that only the class of animals which are the object of the particular kind
of feed produced need be maintained.
• Section 11. Two or more small feed millers may agree among themselves to establish and
maintain a common quality contract laboratory and retain the services of a common
personnel therefore and such shall be considered sufficient compliance to the provisions of
section 8 hereof; provided that in lieu of the above any small feed miller may attach and
avail itself of the laboratory services of any recognized college/institute/university offering
its laboratory for feed quality control services.
• Section 31. Damaged and adulterated feed and feedstuff shall not b sold or offered for sale.
For purposes of this order, the addition of ground rice hull to rice bran is expressly
prohibited.
o Adulterated feeds:
Mixed feeds, feedstuffs or ingredients found to contain any material that
may be injurious, damaged or of no food value.
Substance to increase bulk or weight and/or may reduce its quality or
strength.
Mixture of two or more mixed feeds of different formula or brand with
intent to sell.
o Article IV. Classification
Rice by-products:
Rice polish is the finely powdered material obtained in polishing rice
kernels. It shall have the following analysis:
CP – 12.0% min
Fat – 15.0% min
Fiber – 6.0% max
Moisture – 13.0% max
Rice bran is the pericarp of bran layer of rice, with only such quantity
of full fragments as is unavoidable in the regular milling of rice. D1
– 1st class – fine rice bran
CP – 11.0% min
Fat – 12.0% min
Fiber – 7.0% max
Moisture – 13.0% max
Rice bran is the pericarp of bran layer of rice, with only such quantity
of full fragments as is unavoidable in the regular milling of rice. D2
– 2nd class – coarse rice bran
CP – 4.0% min
Fat – 2.0% min
Fiber – 12.0% max
Moisture – 13.0% max
Corn by-products:
 Corn bran is the outer coating of the corn kernel, with little or none of the
starchy part of germ. It shall have the following analysis:
CP – 10.0% min
Fat – 5.0% min
Fiber – 8.0% max
Moisture – 13.0% max
Corn grits are hard portions of corn, with little or none of the bran or
germ. CP – 7.0% min
Fat – 0.5% min
Fiber – 2.0% max
Moisture – 13.0% max
Wheat by-products
Hard wheat pollard is that portion of the wheat bran between the skin
or the bran and the white interior (source of white flour).
CP – 16.0% min
Fat – 3.0% min
Fiber – 8.0% max
Moisture – 13.0% max
Soft wheat pollard is that portion of the wheat bran between the skin
or the bran and the white interior (source of white flour)
CP – 12.0% min
Fat – 4.0% min
Fiber – 8.0% max
Moisture – 13.0% max

Method of Analysis
• Section 23. The method of analysis as published in the official methods of the Association
of Official Agricultural Chemists (AOAC), latest edition, shall be adopted in making
analysis.

Prohibitions
• Damaged and adulterated feeds/feed ingredients shall not be sold
• No custom – mixed feed shall be sold in the open market
• Containers which have been previously used for things or objects harmful to animals shall
not be used as containers for feed or feedstuffs

Facilities/ Equipment for QC Laboratory

• Small Feedmill o 1 mixer (500
kg/batch) o Operation – not
regular o Requirement:
Moisture analyzer
Set of sieves
Stereomicroscope
Test kits (urease activity)
Weighing balance

• Medium Feedmill o 1 mixer (1-2

T/batch) o Operation on regular
basis o Additional requirement:
Plus, facilities for proximate analysis, calcium, phosphorus and salt

• Large Feedmill o Mixer (1-4

T/batch) o Operation: NLT 8
hrs/day o Additional requirement
Plus, purity of vitamins/drugs concentration of trace minerals,
microbiological assay
• Multi-unit Feedmill o More than
2 units mixer (1-4 T/batch) o
Operation: > 8 hrs/day o
Requirement:
Advanced instrumental facilities such as HPLC, NIR, bomb calorimeter,
etc.