Managemental Diseases in Poultry Part 1

 There are different managemental diseases in Poultry. we will discuss these diseases step by step.

Ventral Prolapse

Egg Bound

Vent Pecking

Ventral Prolapse:

Ventral prolapse is (also known as Oviduct Prolapse, Blowout, Cloacal Prolapse and Pick out) a condition in which lower part of hen's oviduct turns inside out and protrudes through the vent. Prolapse is very serious condition that can be treated if diagnose early, but is likely to recur. 

Causes:

1.   Imbalance Weight:

Under Weight Birds:

    Birds with smaller BW during 3-6 weeks of age, upon reaching maturity have smaller skeletal frame, smaller cloacal diameter. when egg is laid the hen exerts force due to which injuries occur in cloacal muscles. Oviduct come out of cloaca and fail to retract. sometimes oviduct is also accompanied by intestines.

Overweight Birds:

    Overweight in 10-15 weeks of age when photo-stimulated produce larger eggs than the standard. this leads to rupture of cloacal muscles and results in prolapse.

2. Over Photo-stimulation:

    Birds at 13-15 weeks are over photo-stimulated by high intensity and longer duration particularly in under weight birds. Instead of multiple increments of short periods of light duration more light is given in short time. The birds body weight lags its egg production and narrow cloaca is inflicted with injuries leading to Prolapse. 

High light intensity more than 50 lux in open sided houses. More than 15 lux in light-controlled houses also causes Ventral Prolapse. 

3. High Energy High Protein Feed:

    Egg production and size develops at faster rate and larger eggs lead injuries to the cloacal muscles causing Prolapse.

4. Minerals and Vitamin Deficiency:

Calcium Deficiency (Calcium Tetany):

    Birds come into production at a faster rate and lower feed intake causes Ca deficiency in birds. It leads to contraction of cloacal muscles (Ca Tetany). Lesser dilation of cloacal muscles results in injuries and tears of cloacal wall leading to prolapse.

Vit. D3, Phosphorus Deficiency:

    Leads to lesser absorption of Ca.

Prevention and Treatment:

1. Do not overstimulate the birds by increased light duration and intensity.

2. Maintain the BW as per standards of Breed particularly in 3-6 week of age.

3. Do not overweight the birds from 12-16 weeks of age.

4. Provide extra Calcium during peak production. 

5. Do not give high protein high energy feed during production.

A Review about different clays as toxin Binders

 

There are different types of clays like Bentonite, Clinoptilolite, Kaolinite etc. in the market, which are used as toxin binders. Each caly binds aflatoxins and some ochratoxins. But each clay has its own properties and drawbacks.

In this blog we will study the properties and flaws of all clays which are used in the industry as toxin binder.

Bentonite:

Bentonites are the clay rocks altered from glassy igneous material such as a volcanic ash or tuff. Bentonites have been used as palletizing iron ores, foundry bond clay, ceramic, drilling mud, sealant, animal feed bond, bleaching clay, agricultural carrier, cat box adsorbent, adhesive, catalyst and catalyst support, desiccant, emulsion stabilizer, cosmetic, paint, pharmaceutical, civil engineering, clay organoclay and polymer-clay nanocomposites.

    Bentonites are greatly affected from the acid activation, ion exchange, heating and hydrothermal treatments, and some other physicochemical processes. For example, physicochemical properties such as strength, swelling, plasticity, cohesion, compressibility, particle size, cation-exchange capacity, pore structure, surface area surface acidity and catalytic activity as well as the mineralogy can change considerably by modifications.

    Commercial importance of bentonites depends on the contents of their clay and nonclay minerals. Dominant clay minerals in bentonites are smectites such as montmorillonite, beidellite, saponite, nontronite and hectrorite. Bentonites are seldom found as monomineralic clays and may contain other clay and nonclay minerals and also some organic impurities.

Structures of Smectite:

    Smectite is a 2:1 layer clay mineral and has two silica tetrahedral bonded to a central alumina octahedral (O) sheet as seen in Fig. 2:

    The net negative charge of the 2:1 (TOT) layers arising from the isomorphic substitution in the octahedral sheets of Fe²⁺ and Mg²⁺ for Al³⁺ and in tetrahedral sheets of Al³⁺ for Si⁴⁺ is balanced by the exchangeable cations such as Na⁺, and Ca²⁺ located between the layers and around the edges. The mineral is called Na- smectite (NaS) or Ca-smectite (CaS) corresponding to the exchangeable cation which in Na⁺ or Ca²⁺. Industrial bentonites predominantly contain either Na-montmorillonite or Ca-montmorillonite. The equivalent amount of exchangeable cations in one kilogram smectite as well as other clay minerals and clays is defined cation exchange capacity (CEC).

Swelling:

                The physical state of smectite and corresponding bentonite may be changed with increasing water content, from anhydrous solid to a hydrated material, semi-rigid plastic, gel and suspension respectively.

                The change in the physical state of a bentonite from an anhydrous solid to gel is called swelling. The swelling of smectites occurs between the 2:1 (TOT) layers in agglomerated particles.

Porous Structure:

Smectites are porous clay minerals. The voids in a solid located amoung and within particles are caleed pore. The shape of the pores having different sizes can be cylindrical, parallel-sided slit, wedge, cavity and ink-bottle.

Adsorption Non-Polar Molecules:

                Smectites and other clay minerals do not adsorb non-polar molecules such as nitrogen, argon and ethane at elevated temperatures. These molecules can be adsorbed on smecitites at their liquefaction temperatures but cannot penetrate between the 2:1 (TOT) layers.

Adsorption Polar Molecules:

    A montmorillonite consists of 15-20 elements. Between the different elements, there are cations (next to crystal water), which are easy to be exchanged by other cations or positively charged molecules.

The cation exchange capacity (CEC Value) describes the capacity of clay minerals to exchange cations.

 

Clinoptilolite (Zeolite):

    Clinoptilolite is a natural zeolite composed of a microporous arrangement of silica and alumina tetrahedral. Among a high number of natural zeolites, clinoptilolite is best known. Zeolites are classified as tectoaluminosilicates with large pores and channels in the structures containing loosely bound water molecules (so called zeolite water) and alcalic cations (Na⁺, K⁺, Li⁺ Cs⁺, Ca²⁺, Mg²⁺, Ba²⁺, Sr²⁺). They can selectively adsorb gas and steam molecules, reversibly adsorb and desorb water, or based on ion selectivity they can exchange own cations for other ones.

     Zeolites are also used as effective adsorbents of toxic agents, particularly aflatoxins from the feed. They effectively minimize adverse effects of aflatoxins on feed intake, performance and nutrient conversion, and reduce mycotoxin concentration in the livers of affected animals. A lower concentration (15g/kg) of zeolite in the diet seems more effective than a higher concentration (25g/kg) as it was describe by Oguz snf Kurtoglu.

    Zeolite supplemented diets are well tolerated by the animals; they support biomas production and improve the health status of the animals.  Clinoptilolite in the diet of layer hens (50g/kg) increased the number of laid eggs, stability of eggshell and efficiency of food utilization; however, neither the onset of the egg lay cycle, nor egg weight were affected (Olver, 1997).

Kaolin:

    Kaolin is a plastic raw material, particularly consisting of the clay mineral kaolinite. The chemical formula is Al₂O₃.2SiO₂.2H₂O (39.5% Al₂O₃, 46.5% SiO₂, 14.0% H₂O). Kaolinite ranks among phyllosilicates, are classified into the main groups according to the type of the layers, interlayer content, charge of the layers and chemical formulas.

Structure of Kaolinite clay

Physical Properties:

                The 1:1 platelets of kaolinite are held together strongly via hydrogen bonding between the OH of the octahedral layer and the O of the tetrahedral layer. Due to this strong attraction these platelets do not expand when hydrated and kaolinite only has external surface area. Also, kaolinite has very little isomorphic substitution of Al for Si in the tetrahedral layer. Accordingly, it has a low cation exchange capacity. Kaolinite easily adsorbs water and forms a plastic, paste-like substance.

Happy Teachers Day

 

Bovine Ephemeral Fever (Three Days Sickness Disease)

 

Three Days Sickness Disease

Key Points

• Bovine ephemeral fever is a disease of cattle and water buffalo caused by a rhabdovirus and transmitted by flying, biting insects.

• Because of the inflammatory nature of the disease, NSAIDs are very effective at relieving clinical signs and pain.

• Vaccine effectiveness varies. Inactivated vaccines provide only short-term immunity and should be administered at least three times to gain some effectiveness in prevention of clinical signs.

Bovine ephemeral fever (also known as 3 days sickness disease) is an arthropod-borne viral disease of cattle and water buffalo that causes milk production losses, recumbency, and sometimes death.

Bovine ephemeral fever is an insect-transmitted, noncontagious, viral disease of cattle and water buffalo that is seen in Africa, the Middle East, Australia, and Asia. Inapparent infections can develop in Cape buffalo, hartebeest, water-buck, wildebeest, deer, and possibly goats, sheep, and gazelles. Low levels of antibody have been recorded in several other antelope species, giraffe, and even in pigs and elephants, but the specificity has not been confirmed.

Etiology and Epidemiology

Bovine ephemeral fever virus (BEFV) is classified as a member of the genus Ephemerovirus in the family Rhabdoviridae (single-stranded, negative sense RNA). The virus is ether-sensitive and readily inactivated at pH levels below 5 and above 10. Although BEFV is considered to exist as a single serotype worldwide, antigenic variation has been demonstrated by cross-neutralization tests, monoclonal antibody panels, and epitope mapping. Several closely related ephemeroviruses (including Berrimah virus, Kimberley virus, Malakal virus, Adelaide River virus, Obodhiang virus, Puchong virus, Kotonkan virus, Koolpinyah virus, and Mavingoni virus) have been identified. However, of these, only Kotonkan virus (isolated in Nigeria) has been associated with clinical ephemeral fever in cattle.

BEFV can be transmitted from infected to susceptible cattle by IV inoculation; as little as 0.005 mL of blood collected during the febrile stage is infective. To date, infection by virus obtained from virus culture has never succeeded. Although the virus has been recovered from several Culicoides species and from anopheline and culicine mosquito species collected in the field, the identity of the major vectors has not been proved. Transmission by contact or fomites does not occur. The virus does not appear to persist for long periods in recovered cattle, though it was detected in lymphoid tissue one week after cessation of viremia. Infection results in long term immunity.

The prevalence, geographic range, and severity of the disease vary from year to year, and epidemics occur periodically. During epidemics, onset is rapid; many animals are affected within days or 2–3 weeks. Bovine ephemeral fever is most prevalent in the wet season in the tropics and in summer to early autumn in the subtropics or temperate regions (when conditions favor multiplication of biting insects); it disappears abruptly in winter. Virus spread appears to be associated with winds and transportation of animals. Morbidity may be as high as 80%; overall mortality is usually 1%–2%, although it can be higher in lactating cows, bulls in good condition, and fat steers (10%–30%). However, reported overall mortality rates have exceeded 10% in outbreaks in several countries in recent years.

Clinical Findings

Bovine Ephemeral fever signs occur suddely and vary in severity, which include:

• biphasic to polyphasic fever (40°–42°C [104°–107.6°F])

• shivering

• inappetence

• tearing

• serous nasal discharge

• drooling

• pulmonary emphysema

• increased heart rate

• tachypnea or dyspnea

• atony of forestomachs

• depression

• stiffness and lameness

• a sudden decrease in milk yield

Clinical signs are generally milder in water buffalo. Affected cattle may become recumbent and paralyzed for 8 hours to >1 week. After recovery, milk production can fail to return to normal levels until the next lactation. There are anecdotal reports of abortions. This might be an indirect consequence of the disease, because the virus does not appear to cross the placenta or affect the fertility of the cow. Apparently, bulls, heavy cattle, and high-lactating dairy cows are the most severely affected, but spontaneous recovery usually occurs within a few days. More insidious losses may result from decreased muscle mass and lowered fertility in bulls.

Lesions

Bovine ephemeral fever is an inflammatory disease. The most common lesions include:

• polyserositis affecting pleural, pericardial, and peritoneal surfaces

• serofibrinous polysynovitis, polyarthritis, polytendinitis, and cellulitis

• focal necrosis of skeletal muscles

Histomorphologic abnormalities in peripheral nerves and brain have been detected as well. Generalized edema of lymph nodes and lungs, as well as atelectasis, also may be present.

Diagnosis

• Clinical signs

• PCR identification of the virus

Diagnosis of bovine ephemeral fever is based almost entirely on clinical signs in an epidemic. Whole blood should be collected from sick and apparently healthy cattle in affected herds and must be sufficient to provide two air-dried blood smears, 5 mL of whole blood in anticoagulant (not EDTA), and ~10 mL of serum. A differential WBC count on blood smears can either support or refute a presumptive field diagnosis. The majority of clinical cases have a neutrophilia with the presence of many immature forms, although this is not pathognomonic. Plasma fibrinogen rises on the day of peak fever and remains elevated for at least 7 days. Hypocalcemia may occur one day after fever onset.

Timely laboratory confirmation is mostly performed by PCR and rarely by virus isolation. Serum neutralization is diagnostic in retrospect. A 4-fold rise in antibody titer between paired sera collected 2–3 weeks apart confirms infection.

Virus is best isolated by inoculation of mosquito (Aedes albopictus) cell cultures with defibrinated blood, followed by transfer to baby hamster kidney (BHK-21 or BHK-BSR) or monkey kidney (Vero) cell cultures after 15 days. Suckling mice may also be used for primary isolation by intracerebral inoculation. Isolated viruses are identified by PCR and sequencing, neutralization tests using specific BEFV antisera, and ELISA using specific monoclonal antibodies.

Treatment and Control

• NSAIDs

• Supportive care for recumbent cows

Complete rest is the most effective treatment for bovine ephemeral fever, and recovering animals should not be stressed or worked because relapse is likely. Anti-inflammatory drugs given early and in repeated doses for 2–3 days are effective. Oral dosing should be avoided unless the swallowing reflex is functional. Signs of hypocalcemia are treated as for milk fever. Antibiotic treatment to control secondary infection and rehydration with isotonic fluids may be warranted.

There is conflicting evidence regarding the effectiveness of the commercially available attenuated or inactivated BEFV vaccines. Although an attenuated BEF vaccine showed high effectiveness in Australia, reports from other countries indicate lower effectiveness of the same vaccine. Inactivated virus vaccines have not produced longterm protection against experimental challenge with virulent virus and cannot guarantee lasting immunity. In field studies, they were 50% effective only after at least three vaccinations. Although a subunit vaccine that protects against field and laboratory challenge has been described, it is not commercially available. The efficacy of vector control remains uncertain, because the insect vectors have not been fully identified. There is no evidence that people can be infected.

Metabolic Disorders (Ketosis in Cattle)

Ketosis is a common disease of adult cattle. It is also known as Acetonemia or Ketonemia. It typically occurs in dairy cows in early lactation and is most consistently characterized by partial anorexia and depression. Rarely, it occurs in cattle in late gestation, at which time it resembles pregnancy toxemia of ewes. In addition to inappetence, signs of nervous dysfunction, including pica, abnormal licking, incoordination and abnormal gait, bellowing, and aggression, are occasionally seen. The condition is worldwide in distribution but is most common where dairy cows are bred and managed for high production.

Etiology & Pathogensis:

The pathogenesis of bovine ketosis is incompletely understood, but it requires the combination of intense adipose mobilization and a high glucose demand. Both of these conditions are present in early lactation, at which time negative energy balance leads to adipose mobilization, and milk synthesis creates a high glucose demand. Adipose mobilization is accompanied by high blood serum concentrations of nonesterified fatty acids (NEFAs). During periods of intense gluconeogenesis, a large portion of serum NEFAs is directed to ketone body synthesis in the liver. Thus, the clinicopathologic characterization of ketosis includes high serum concentrations of NEFAs and ketone bodies and low concentrations of glucose. In contrast to many other species, cattle with hyperketonemia do not have concurrent acidemia. The serum ketone bodies are acetone, acetoacetate, and β-hydroxybutyrate (BHB).

There is speculation that the pathogenesis of ketosis cases occurring in the immediate postpartum period is slightly different than that of cases occurring closer to the time of peak milk production. Ketosis in the immediate postpartum period is sometimes described as type II ketosis. Such cases of ketosis in very early lactation are usually associated with fatty liver. Both fatty liver and ketosis are probably part of a spectrum of conditions associated with intense fat mobilization in cattle. Ketosis cases occurring closer to peak milk production, which usually occurs at 4–6 wk postpartum, may be more closely associated with underfed cattle experiencing a metabolic shortage of gluconeogenic precursors than with excessive fat mobilization. Ketosis at this time is sometimes described as type I ketosis.

The exact pathogenesis of the clinical signs is not known. They do not appear to be associated directly with serum concentrations of either glucose or ketone bodies. There is speculation they may be due to metabolites of the ketone bodies.

Epidemiology:

All dairy cows in early lactation (first 6 wk) are at risk of ketosis. The overall prevalence in cattle in the first 60 days of lactation is estimated at 7%–14%, but prevalence in individual herds varies substantially and may exceed 14%. The peak prevalence of ketosis occurs in the first 2 wk of lactation. Lactational incidence rates vary dramatically between herds and may approach 100%. Ketosis is seen in all parities (although it appears to be less common in primiparous animals) and does not appear to have a genetic predisposition, other than being associated with dairy breeds. Cows with excessive adipose stores (body condition score ≥3.75 out of 5) at calving are at a greater risk of ketosis than those with lower body condition scores. Lactating cows with subclinical ketosis are also at a greater risk of developing clinical ketosis and displaced abomasum than cows with lower serum BHB concentrations.

Clinical Findings:

In cows maintained in confinement stalls, reduced feed intake is usually the first sign of ketosis. If rations are offered in components, cows with ketosis often refuse grain before forage. In group-fed herds, reduced milk production, lethargy, and an “empty” appearing abdomen are usually the signs of ketosis noticed first. On physical examination, cows are afebrile and may be slightly dehydrated. Rumen motility is variable, being hyperactive in some cases and hypoactive in others. In many cases, there are no other physical abnormalities. CNS disturbances are noted in a minority of cases. These include abnormal licking and chewing, with cows sometimes chewing incessantly on pipes and other objects in their surroundings. Incoordination and gait abnormalities occasionally are seen, as are aggression and bellowing. These signs occur in a clear minority of cases, but because the disease is so common, finding animals with these signs is not unusual.

Diagnosis:

The clinical diagnosis of ketosis is based on presence of risk factors (early lactation), clinical signs, and ketone bodies in urine or milk. When a diagnosis of ketosis is made, a thorough physical examination should be performed, because ketosis frequently occurs concurrently with other peripartum diseases. Especially common concurrent diseases include displaced abomasum, retained fetal membranes, and metritis. Rabies and other CNS diseases are important differential diagnoses in cases exhibiting neurologic signs.

Cow-side tests for the presence of ketone bodies in urine or milk are critical for diagnosis. Most commercially available test kits are based on the presence of acetoacetate or acetone in milk or urine. Dipstick tests are convenient, but those designed to detect acetoacetate or acetone in urine are not suitable for milk testing. All of these tests are read by observation for a particular color change. Care should be taken to allow the appropriate time for color development as specified by the test manufacturer. Handheld instruments designed to monitor ketone bodies in the blood of human diabetic patients are available. These instruments quantitatively measure the concentration of BHB in blood, urine, or milk and may be used for the clinical diagnosis of ketosis.

In a given animal, urine ketone body concentrations are always higher than milk ketone body concentrations. Trace to mildly positive results for the presence of ketone bodies in urine do not signify clinical ketosis. Without clinical signs, such as partial anorexia, these results indicate subclinical ketosis. Milk tests for acetone and acetoacetate are more specific than urine tests. Positive milk tests for acetoacetate and/or acetone usually indicate clinical ketosis. BHB concentrations in milk may be measured by a dipstick method that is available in some countries, or by the electronic device mentioned above. The BHB concentration in milk is always higher than the acetoacetate or acetone concentration, making the tests based on BHB more sensitive than those based on acetoacetate or acetone.

Treatment:

Treatment of ketosis is aimed at reestablishing normoglycemia and reducing serum ketone body concentrations. Bolus IV administration of 500 mL of 50% dextrose solution is a common therapy. This solution is very hyperosmotic and, if administered perivascularly, results in severe tissue swelling and irritation, so care should be taken to ensure that it is given IV. Bolus glucose therapy generally results in rapid recovery, especially in cases occurring near peak lactation (type I ketosis). However, the effect frequently is transient, and relapses are common. Administration of glucocorticoids, including dexamethasone or isoflupredone acetate at 5–20 mg/dose, IM, may result in a more sustained response, relative to glucose alone. Glucose and glucocorticoid therapy may be repeated daily as necessary. Propylene glycol administered orally (250–400 g/dose [8–14 oz]) once per day acts as a glucose precursor and is effective as ketosis therapy. Indeed, propylene glycol appears to be the most well documented of the various therapies for ketosis. Overdosing propylene glycol leads to CNS depression.

Ketosis cases occurring within the first 1–2 wk after calving (type II ketosis) frequently are more refractory to therapy than cases occurring nearer to peak lactation (type I). In these cases, a long-acting insulin preparation given IM at 150–200 IU/day may be beneficial. Insulin suppresses both adipose mobilization and ketogenesis but should be given in combination with glucose or a glucocorticoid to prevent hypoglycemia. Use of insulin in this manner is an extra-label, unapproved use. Other therapies that may be of benefit in refractory ketosis cases are continuous IV glucose infusion and tube feeding.

Prevention and Control:

Prevention of ketosis is via nutritional management. Body condition should be managed in late lactation, when cows frequently become too fat. Modifying diets of late lactation cows to increase the energy supply from digestible fiber and reduce the energy supply from starch may aid in partitioning dietary energy toward milk and away from body fattening. The dry period is generally too late to reduce body condition score. Reducing body condition in the dry period, particularly in the late dry period, may even be counterproductive, resulting in excessive adipose mobilization prepartum. A critical area in ketosis prevention is maintaining and promoting feed intake. Cows tend to reduce feed consumption in the last 3 wk of gestation. Nutritional management should be aimed at minimizing this reduction. Controversy exists regarding the optimal dietary characteristics during this period. It is likely that optimal energy and fiber concentrations in rations for cows in the last 3 wk of gestation vary from farm to farm. Feed intake should be monitored and rations adjusted to meet but not greatly exceed energy requirements throughout the entire dry period. For Holstein cows of typical adult body size, the average daily energy requirement throughout the dry period is between 12 and 15 Mcal expressed as net energy for lactation (NE_L). After calving, diets should promote rapid and sustained increases in feed and energy consumption. Early lactation rations should be relatively high in nonfiber carbohydrate concentration but contain enough fiber to maintain rumen health and feed intake. Neutral-detergent fiber concentrations should usually be in the range of 28%–30%, with nonfiber carbohydrate concentrations in the range of 38%–41%. Dietary particle size will influence the optimal proportions of carbohydrate fractions. Some feed additives, including niacin, calcium propionate, sodium propionate, propylene glycol, and rumen-protected choline, may help prevent and manage ketosis. To be effective, these supplements should be fed in the last 2–3 wk of gestation, as well as during the period of ketosis susceptibility. In some countries, monensin sodium is approved for use in preventing subclinical ketosis and its associated diseases. Where approved, it is recommended at the rate of 200–300 mg/head/day.

x

Recent Trends in Feed Assessment

 Professor Dr. Ravi Ravindran* says that “Feed assessment is the basis for feed formulation and routine feed evaluation offers critical highlights”. Matrix values need to be updated and to bring nutrient supply closer to target requirements, lower nutrient wastage into environment and improve sustainability.

Introduction:

Routine and proper ingredient evaluation is central to precise and cost-effective feed formulations. The matrix values used in formulations, whether from tabular values, prediction equations or research data, are based on ingredient evaluation research. The aim of feed evaluation is to provide the nutritionists with reliable data on the variability in digestible and metabolisable nutrient contents in feed ingredients, so that the variation within ingredients could be incorporated into matrix values. Furthermore, the predicted future growth of the poultry industry will have a profound effect on the demand for ingredients and search for ‘alternative raw materials’. When using such poorly digested alternative ingredients, formulation based on digestible nutrients is a requisite and, better feed evaluation practices become even more pertinent.

Basic principles of poultry feed evaluation:

Two fundamental features from the basis of feed evaluation in poultry.

Ileal digestibility:

First, it is well accepted that determination of digestibility of nutrients in poultry should be based on the analysis of ileal digesta. The only exception is the determination of apparent metabolizable energy (AME), which involves total collection of excreta and the metabolisability is calculated as the difference between dietary energy input and excreta energy input. 

Composition of assay diets:

Second, three different methodologies (direct method, difference method and regression), varying in the composition of assay diets, are used in digestibility assessments of a nutrient. None of these methods are prefect and, each methodology has its own strengths and weaknesses.

Protein evaluation:

During the past 30 years, the basis of feed formulation has slowly shifted from total amino acids (AA) to the digestible AA system, which has enabled us to meet AA requirements more precisely and to increase the range and inclusion levels of alternative ingredients, while maintaining performance levels. Initially, AA digestibility measurement was based on excreta analysis. During the 1980’s, the precision-fed rooster assay was popular but this assay has since lost global acceptance because of ethical issues. 

Currently, use of ileal-based broiler digestible AA is widely accepted. Considerable published data have now become available on the ileal AA digestibility of raw materials. A major issue with these data however, is the wide variability reported in digestibility estimates. There are two sides to the observed variation namely, (i) inherent variability expected in raw materials and (ii) the differences arising from methodological differences employed in different research stations. The latter is a real concern. Results from a collaborative study, involving three research stations, exemplifies the variability that may occur due to differences in assay procedures (Table 1).

Table 1: Apparent ileal digestibility coefficients of crude protein and select amino acids in maize determined at three research stations, using station protocols.

	Station 1	Station 2	Station 3	SEM	p≤
Crude protein	0.73	0.85	0.80	0.027	0.05
Lysine	0.63	0.83	0.79	0.036	0.05
Methionine	0.84	0.92	0.86	0.029	0.16
Threonine	0.62	0.77	0.73	0.023	0.05
Average1	0.76	0.87	0.83	0.030	0.05

1Average of 17 amino acids

In a follow-up study, which used a common agreed protocol, the between station variation was eliminated. These results highlight the need for a consensus protocol for use not only in the measurement of digestibility of AA, but of all nutrients to enable better comparison of data generated across research stations working in ingredient evaluation.

Confusion about the terminology used to describe the AA digestibility estimates becomes clear to anyone perusing the available digestibility data. For each AA, there are at least six possible values, and combinations thereof, to describe the digestibility for poultry: apparent or true or standardized; rooster or broiler; and excreta or ileal. Many end-users often do not know which values are being used in their matrixes. Currently, the term ‘standardized ileal digestibility (SID)’is being increasingly used in the poultry industry. Compared to other terms, SID is the one relevant to the way we formulate diets. It is additive and aligned with the ideal protein concept.

Energy evaluation:

The use of appropriate energy system is another critical issue because of the importance of energy to bird performance and diet cost. An ideal energy system must be easy to measure, predictive of bird performance, additive in feed formulations and independent of bird factors. However, energy metabolism is too complex to meet all these ideals. 

Since the 1950’s, apparent metabolizable energy (AME) has been the system of choice of describing available energy for poultry. True metabolizable energy became popular in the 1980’s but has since lost favor owing to ethical issues. Currently, the AME is the widely accepted system to describe favoured system in the foreseeable future. It is not a perfect system, with several limitations (Table 2). However, it is familiar and universal, and its limitations are overlooked.

Table 2: Limitations of AME

Ingredient values may not be additive in formulations

Variations in published data due to: Methodology differences, including bird factors (age, gender, production stage) Ingredient factors

Does not take account of energy lost as heat

Net energy (NE) system, a refinement of the AME concept, has received attention from time to time. In theory, NE will more closely describe the energy available in an ingredient for bird’s metabolic functions and is more predictive of animal performance. It is, however, difficult to assay, costly and time consuming. To be acceptable, its economic advantage over the AME system needs to be demonstrated.

Phosphorus evaluation:

Globally there are growing concerns about phosphorus (P) excretion from intensive animal operations into the environment. Gradual depletion of global feed phosphates deposits is another concern. These issues are driving research into P digestibility in order to efficiently use and conserve the finite P resources.

A related issue is the considerable confusion that exists regarding the terminology to describe P that is available to the bird (e.g. available P, non-phytate P and retain-able P). Use of a sound criterion to assess P availability. One key finding from recent research is that, contrary to common premise, non-phytate P does not equate to digestible P suggesting that broilers are able to utilize a portion of phytate-bound P in feed ingredients.

Calcium evaluation:

Measurement of Ca digestibility in poultry has received relatively little attention in the past due to the cheap availability of limestone, the major source of Ca in poultry diets. However, the move towards a digestible P system necessitates a closer look at digestible Ca because of the close relationship between Ca and P during and after absorption.

It is widely assumed that Ca in common Ca sources (limestone, meat and bone meal, dicalcium phosphate) is highly available, but recent studies have shown that this is not true (Table 3).

Table 3: True digestibility of calcium of feed ingredients (%).

Feed ingredient	Calcium digestibility (%)
Meat and bone meal	50 (range, 41-60)
Limestone	55 (range, 43-71)
Dicalcium phosphate	35 (range 28-45)
Monocalcium Phosphate	35 (range, 32-45)
Canola meal	30
Fish meal	25
Poultry by-product	30

 Sources: Naveed Anwar (2017), Phd Thesis; Laura David (unpublished PhD thesis)

In Vitro methods:

Simple in vitro digestion assays have the potential to yield useful indication of nutrient digestibility (Table 4).

Table 4: Pros and cons of in vitro assays:

Limitations	Value
Not possible to accurately simulate the complex in vivo biochemical and physiological processes	Screening of feed additivies
Anti-nutritional factors, dietary dry matter and fiber, endogenous protein secretions, activity of gut enzymes, and gut bacteria not mimicked in vitro	Ranking of feedstuffs by digestibility
Assays should include lipases, carbohydrases etc. as these affect release of proteins from food matrix	Predicting in vivo nutritive value directly or in combination with measures of chemical constituents

Digestion and absorption processes in the animal, however, are too complex and simulation in laboratory is not possible. Nevertheless, the use of in vitro techniques is attractive because such assays are relatively simple, rapid and reproducible, and avoid the use of animals. While in vitro data are useful scrrening samples, they cannot be used in practical feed formulations.

Near-infrared relectance spectroscopy (NIRS):

Many feed mills routinely use NIRS technology to predict the protein moisture, fat, and ash contents of feed ingredients on an on-going basis. The investment on rapid tests, however, should be extended to the measurement of AME or digestible nutrients (especially digestible AA) to formulate the diets precisely. The success of NIRS in ruminant nutrition suggests that the NIRS is capable of predicting energy values for poultry, but it remains to be seen if this is practically feasible.

By:

*Dr. Ravi Ravindran (V.Ravindran@massey.ac.nz) is Professor of Poultry science with the Monogastric Research Centre, Massey University New Zealand.