Clinical Nutrition in Poultry Production

Ram Singh Bibyan, Priyanka Patir, Lovely Anant, Harneet Kour, Balaga Sravani, Yamini Khatri, Simran Kamboj, Sarita Yadav1, Prajakta Kailas Kangale,  Somesh Rameshrao Gaikwad, Jannat Saini, Sruthy Ravi* and Kanmoni Goyari*

Animal Nutrition Division

ICAR- National Dairy Research Institute

Karnal-132001 (Haryana) India

carirsingh@yahoo.co.in; +91-9457602079

1Senior Scientist

*PhD Scholar; IVRI, Izatnagar

The relationship between nutrition and disease has been known for centuries. According to World Health Organization (WHO), malnutrition (undernutrition and overnutrition) is the ‘cellular imbalance between supply of nutrients and energy and the body’s demand for them to ensure growth, maintenance and specific functions’, and is the greatest risk factor for illness and death worldwide. Due to proper nutrition, dramatic advancement has been witnessed in the bird’s performance in terms of weight gain and reduction in market age approximately by one day each year. In 1976, it took 63 days for a commercial broiler to attain a market weight of 2 kg; and in 2008, it is just about 34 days for the same weight with a FCR of 1.5 to 1.7. Similarly, egg production in commercial layers has been increased to 325 eggs with reduction of feed intake of 122-125g per egg from 130g/ egg. Even then poultry industry has crippled many times due to rising feed cost, fluctuating market price of broiler meat and eggs, and pre-harvest losses due to emerging of new or re-emerging of existing diseases causing great mortality and unaccountable morbidity. However, this vivid progress of growth in body weight of broilers (50 fold just in 34 days) and egg production has led to production stress, immune-insufficiency, and incidence of more diseases. The birds are periodically vaccinated but the control measure through vaccination alone has also proved many times ineffective. Therefore, the present strategies towards control of diseases have been a joint approach including vaccination programmes, selective breeding for augmenting disease resistance capacity of birds, improved management to curtail environmental stress to a minimum level, and nutritional approaches. The different clinical areas that have received due attention in the field of nutrition for augmenting poultry production and welfare include: Understanding interaction of nutrition and infection; identifying nutrients for improved immuno-responsiveness; nutritional management of mycotoxicosis; extrinsic and intrinsic toxic factors; their role in health and immunity, feeding management affecting health and immunity, identifying feed additives for health and immunity; and controlling emerging diseases due to high plane of nutrition.

Interaction of nutrition and infection: Interaction means the response of one or more nutrients towards the artificially induced or naturally occurring disease/ infection. It also includes the nutritional impairment caused by an infection. Nutrition of the host may interact with pathogens either synergistically or antagonistically. In synergistic cases, the impaired nutritional status of the host tends to decrease the resistance to a pathogen. Sometimes impaired nutrition may also protect the host against the virulence of a pathogen, or infection may improve the nutritional status of the host (antagonism). Higher nutritional plane in order to achieve maximum gain has also led to emergence of certain diseases of growing chicks and poults. Not a single nutrient acts prophylactically against infection. However, the course of the diseases can be altered by nutrition. Again nutrition does not influence all infections equally and all nutrients do not have similar influence to a particular infection.

Protein and Energy: The body uses the energy-yielding nutrients to fuel all its activities. When the body uses carbohydrate, fat, or protein for energy, the bonds between the nutrient’s atoms break. As the bonds break, they release energy. Some of this energy is released as heat, but some is used to send electrical impulses through the brain and nerves, to synthesize body compounds, and to move muscles. The fatality rate of chickens following inoculation with Salmonella gallinarum increased with the increasing dietary protein level, while, chicks fed low (15%) protein had higher fatality than those fed high (30%) protein on inoculation with E. coli. Severity of E. coli infection was higher in chicks fed diets of high nutrient density. Excessive low (CP, 8%) or high protein (CP, 41%) diets increased severity of Newcastle disease. However, growth depression was less in chicks infected with Newcastle disease virus with lysine deficient than on control diet. Feeding diets containing 0-30% CP before inoculation with Eimeria, fatality increased progressively upto 15% CP. Chicks artificially infected with E. tenella and fed 24% protein in diet suffered high mortality than those fed 16 or 20% CP. However, in E. acervulina infection higher protein was beneficial to protect weight loss. After a natural outbreak of intestinal coccidiosis, a high protein diet seemed more beneficial. Diet supplemented with 4% fish oil attenuated the growth depression effect of E. tenella.

Vitamins: Addition of vitamin A in diet of chickens suffering from Mycobacterium tuberculosis or infected with E coli, improved survival rate, this effect was attributed to increased antibody production and phagocytosis. Fatality rate increased on inoculation ND virus in chicks receiving borderline vitamin A deficient diet. Pre-existing marginal vitamin A status increased the severity of Newcastle disease and following infection, the plasma vitamin A reduced to a level regarded as deficient. Following Infectious bronchitis infection, the birds receiving 3600 or 10000 IU of vitamin A per lb of diet experienced greater live weight during active disease condition. Supplemental vitamin A in diet over normal level did not reduce mortality or morbidity but helped the Eimeria infected chicks to recover faster. Supplementation of vitamin D3 @ 2064 IU/kg reduced the incidence of turkey osteomyelitis complex. Addition of 150-300 mg vitamin E/kg diet provided increased protection against E. coli infection in birds. The vitamin E deficient chicks appeared slightly less susceptible to avian encephalomyelitis (AE) virus compared to those fed on control diet. Supplementation of selenium @ 0.25 mg/kg or vitamin E @ 100 mg/kg diet reduced mortality and increased body weight gain of non-immunised chicks infected with E. tenella. Mortality due to E. tenella and E. necatrix infections was reduced on supplementation of diet with vitamin K (@ 0.53 mg/kg diet) but had no beneficial effect against non-haemorrhagic species of coccidia. Supplementation of vitamin C in diet of chicks increased resistance against infectious bursal disease. Ascorbic acid @ 150 mg per kg diet interacted with coccidiosis to increase feed intake and growth.

Minerals: Excess iron either through injection or iron supplemented diet increased survival rate of S. gallinarum infected chicks, whereas, the chicks on iron deficient diet were more susceptible to S. gallinarum. Iron is also an essential element for growth of pathogenic enteric bacteria. Elevated iron concentrations in drinking water or the feed had been attributed to intestinal proliferation of C. botulinum and subsequent, the occurrence of botulism. Chicks suffering from mixed coccidiosis responded remarkably with increased gain and improved feed conversion efficiency when excess zinc was added to the high calcium (2.0%) diet. Supplementation of diet with extra calcium and zinc on the face of coccidial outbreak was also beneficial in improving feed conversion efficiency. Mortality of chicks from mixed coccidiosis was lower at high calcium (1.98%) and high zinc (93 or 123 ppm) containing diets. Supplementation of phosphorus in the form of disodium phosphate did not prove beneficial for coccidian induced chicks.

Nutrition and immunocompetence: Proper functioning of the immune system depends upon the availability of nutrients, the precursors of cell growth and activity. Impaired nutrition is associated with reduced capacity of host to form specific antibodies; decrease in the phagocytic activity; interference with production of non- specific protective substances; reduced non-specific resistance to bacterial toxins; altered tissue integrity, diminished inflammatory response, collagen formation and wound healing, decreased antibody affinity and complement system; and variable endocrine activity. Immune stimulation decreases appetite and muscle protein accretion, increases metabolic rate, body temperature, and oxidative damage to cells.

Protein and energy: Feeding alterations, imbalance of protein, low energy and high dietary fibre impaired immune competence and disease resistance. The level of dietary energy alone or energy and protein did not alter antibody titre to sheep RBC or weight of lumphoid organs (bursa and spleen) in commercial broilers. Broiler chicks fed higher protein in diet (23% CP) revealed better persistency in antibody production to sheep RBC at 10 or 15d post-injection. However, long term obesity had deleterious consequences for response to sheep RBC antigen, resistence to E. coli and livability. Evidences also exist that methionine is an essential input for proper functioning of the immune system. The immune-competence of growing and laying Japanese quails or broilers improved with increase of methionine in diet. Variations in energy intake may affect immune-competence mainly due to faulty management practices rather diet formulation. Feed restriction for broiler breeders and withholding feed in forced molting practices in layers may affect immune-competence. Feed restriction results higher plasma corticosterone level that decrease immune response, possibly through effect on cytokines. Excessive feeding through forced feeding may also have short-term effects on indicators of humoral immunity. The dietary protein and amino acids required to achieve maximum growth and feed efficiency is generally sufficient to support optimum immunity. Again immune response changes metabolism leading to less growth and thus reduces the need for amino acids.

Minerals: Several minerals alter immune-competence. Deficiency (less than 0.14% Na) or excess of sodium or sodium chloride decreased the humoral immune response of chicks. However, the requirement of these minerals for maximum growth and maximal humoral immunity is similar. Certain trace elements like zinc, iron, copper, manganese and selenium are also important for normal immune function and disease resistance, maintenance and functioning of the immune system.

Extrinsic and intrinsic toxic factors: Addition of rye, wheat and barley to a corn based diet had been shown to increase Clostridium perfringens numbers, induced necrotic enteritis and increased bird mortality. Elevated levels of soluble non-starch polysaccharides (arabinoxylans, -glucans, galactomannans, etc.) increased the activity of fermentative microorganisms in the small intestine in a detrimental manner. The antinutritive factors like trypsin inhibitor, tannins, goitrogens, etc. are associated with improper protein and energy utilization and thus may have immune-suppresive effect. Chickens receiving non-extruded soybean had higher mortality rate due to E. coli infection than those fed extruded soybean meal in diet. The mycotoxins in feed adversely affect the immune system by depressing both the cell mediated and humoral immune response resulting in the lowering of overall defence mechanism of the birds. Aflatoxins have direct effect on both cellular and humoral immunity and, cell mediated response is affected at low levels whereas; high levels affect immunoglobulin production and antibody responses. Trichothecenes affect primarily the cellular immunity response by direct effect on bone marrow, spleen, lymph nodes, thymus and intestinal mucosa. Ochratoxin causes impairment of both cellular and humoral immunity accompanied by atrophy of thymus, lower circulating immunoglobulin and phagocytes. Aflatoxin in diet of birds increased the severity of E. tenella and E. acervulina infections.

Role of feed additives in disease prevention: Certain antibiotics (such as aureomycine), coccidiostats and other therapeutic agents have immune-suppressive effect but reserpine improves the humoral antibody response. Feed grade enzymes capable of hydrolyzing soluble non-starch polysaccharides improved health of birds. Administeration of partially hydrolysed guar gum (PHGG) using endo-D-mannanase prevented colonization of S. enteritides in young chicks and laying hens. Probiotics function either by competitive exclusion of pathogens or by antagonistic activity towards pathogenic bacteria. Lactic acid bacteria or yeast are able to inhibit the growth of bacteria like Salmonella, Clostridia, and E. coli. Probiotics specially Lactobacilli and Bacillus cereus are also important in the development of immunocompetence against enteric infections. Enhanced response of T cell function and enhanced production of IgM against Salmonella was observed in birds treated with L. reuteri. There was stimulation of mucosal immune system with the increases activity of macrophages, lymphocytes and production of IgA on Lactobacilli sp. on intraperitonial injection in hen and mice. Probiotics can also improve the host health. Galacto-oligosaccharides, fructo-oligosaccharides, mannan oligosaccharides and lactose derivatives have been used in poultry. Oligosaccharides may directly inhibit the growth of certain intestinal pathogenic species by increasing the concentration of lactic acid in the lower gut. Microbes are able to attach themselves to the mucosa through recognition of oligosaccharides binding sites on the wall. Moreover, certain oligosaccharides like 1,2-glucooligosaccharides are substrate for beneficial Bifidobacterium spp., at lower tract which favoured their colonization and prevented colonization of Clostridium, Enterobacter, E. coli, Entrococcus, etc.

Feeding management affecting health and immunity: Feed restriction for broiler breeders and with holding feed for forced moulting may affect immune-competence. The chicks shifted from alternate- day to the ad lib feeding were found to be more susceptible to the E. coli infection. Feed withdrawal i.e. starvation before processing of broiler chickens has also been associated with increased colonization by bacterial entero pathogens. The crop serves as a reservoir for Salmonella in chicks and the feed withdrawal increased the number of colonized Salmonella in the crop of broilers. Fasting as practiced in meat-type breeders, increased resistance to deleterious effects of E. coli and E. tenella infections. Feed restriction also enhanced development of endocrine glands and humoral immunoresponsiveness. However, feed restriction causes higher plasma corticosterone levels, which are known to decrease the immune response possibly through cytokines. Therefore, feed restriction for broilers breeder and withholding feed in forced moulting practices may affect immunocompetence. Osteomyelitis outbreaks by Staphylococcus aureus have been found to be associated with severe feed restriction, poor nutrition and overcrowding in turkeys. Flocks of chicks harbouring S. aureus in their yolk sacs at one-day of age may develop staphylococcosis when they are stressed by restricted feeding programmes. Similarly, the feed restriction, common programme in raising of broiler breeders, may play an important role in the development of staphylococcal osteomyelitis and synovitis.

Emerging diseases due to high plane of nutrition: Sudden death syndrome (SDS) has been the major non-infectious cause of death (3-4%) in broiler flocks at any age, particularly between first and 4th week of age. SDS has also been reported in layer breeders, fast growing meat turkeys and turkey hens characterized by good body condition, full digestive tract, congestive lungs, enlarged hearts, oedema in thoracic cavity; and congestive and haemorrhagic atria and ventricle. It is assumed that stress of rapid growth is the cause of this syndrome and the heaviest male birds are mostly affected. Various nutritional factors that have been implicated in affecting this disease include growth rate, dietary proteins and fat, cereal grain, vitamins, minerals and processed feed. Feed restriction (25%), high protein diet (24 vs 19%) in order to promote lean meat, replacement of soybean meal by meat meal, replacement of fat with oil in poultry diet and fortification of wheat-soybean meal based diet with thiamine decreased the rate of mortality due to SDS. However, wheat as substitute for corn in poultry diet and pallet processing of poultry mash or of protein supplements increased the incidence of SDS. Ascites/ pulmonary hypertension syndrome (PHS) causes death in rapidly growing broilers especially during winter. It is characterized by increase in lymph in the peritoneal cavity. The nutritional factors which are reported to be the cause of the syndrome include rapid growth, high energy ration, pelleted feed, high sodium, low phosphorus, hepatotoxins, mycotoxins, furazolidone, vitamin E, selenium deficiency and stress. Abnormal skeletal development is another major problem in commercial broilers associated with fast growth and high plane of nutrition. The most common condition is tibial dyschondroplasia. The disease is characterized by swollen proximal end of tibia without apparent lameness in mild from and painful lameness associated with walking on hocks in acute form. The nutritional factors like dietary protein and amino acid levels, feed ingredients, mycotoxins, electrolyte balance, vitamins specially vitamin D3 and minerals have been reported as the cause of these conditions.

Nutrition, immunity and health of birds are closely related. The impact is more pronounced in high producing stock. Management practices involving host’s nutrition can be a potential component in an integrated approach for controlling infection, which has so far poorly been exploited. Future feeding trials should also incorporate immunological studies alongwith the traditional growth and production criteria. Nutrition may also influence the outcome of disease in infected animals. Therefore, the interaction of infectious diseases with different nutrients alongwith the optimum level of interacting nutrients needs to be established. As the immune- stimulation effects of various nutrients are observed at much higher levels than those actually recommended for optimum production, it is therefore necessary to give due  considerations to the economic aspects of the whole exercise. Metabolic imbalances and stress induced by high nutrient intake need to be considered for fast growing broilers without affecting body weight. There is also a need to consider the nutrition, disease control and flock management together to ensure maximum profitability from poultry production.

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