Animal Nutrition and Feed Technology
Year : 2001, Volume : 1, Issue : 1
First page : ( 19) Last page : ( 38)
Print ISSN : 0972-2963.

Interaction of nutrition and infection in poultry - A review

Mandal A.B.*, Elangovan A.V., Verma S.V.S.

Division of Avian Nutrition and Feed Technology Central Avian Research Institute Izatnagar - 243 122, India

*Reprint request: Dr. A.B. Mandal, Tel: +91-581-447223; Fax: +91-581-447321, E-mail: elangocari@rediffmail.com.

Received:  6  September,  2000.

Abstract

Nutrition is one of the major areas of importance amongst the acquired characteristics in relation to disease resistance. Nutrition of the host may affect pathogenesis either synergistically or antagonistically. In synergistic cases the host's impaired nutritional status tends to decrease the resistance for a pathogen. In antagonistic interaction impaired nutrition protests the host against the virulence of the pathogen, or infection may improve the nutritional status. Not a single nutrient acts prophylactically against infection. However, impaired nutrition is associated with reduced capacity of host to form specific antibodies, decrease in the phagocytic activity, altered tissue integrity, diminished inflammatory response, collagen formation and wound healing, and decreased antibody affinity and complement system. Again nutrition does not influence all infections equally and all nutrients do not have similar influence to a particular infection. Feeding management, different feed additives and toxins may also influence the immunocompetence of the birds. The present review highlights the mainstream research and speculates on areas, which need consideration.

Top

Key words

Disease, Feed toxins, Immunity, Interaction, Nutrients, Probiotics.

Top

Introduction

Nutrition and bacterial infections

The role of dietary protein and bacterial infections in chickens has received the attention of different workers from time to time. Increasing the dietary protein level from 10 to 20 or 30% by employing soybean and casein, increased the fatality rate of chickens following inoculation with Salmonella gallinarum (Hill and Garren, 1961). However, chicks fed 15% protein in diet suffered higher fatality rate than those fed 30% protein on inoculation with E. coli (Boyd and Edwards, 1963). Severity of infection was high in chicks fed diets of high nutrient density (Boa-Amponsem et al., 1991). Similarly, fast growing chicks receiving 24% CP and 3146 kcal ME/kg diet had higher lesion score and mortality than those fed on 20% CP and 2685 kcal ME/kg diet (Praharaj et al., 1997). Deleterious effects of E. coli were also more on high plane of nutrition. In another experiment (Nitsan et al., 1989), chickens receiving extruded soybean had lower mortality rate than those fed non-extruded soybean meal in diet. Survival rate of Salmonella gallinarum infected chicks increased when the birds received excess iron either through injection or iron supplemented diet (Hill and Smith, 1974). Whereas, the chicks receiving iron deficient diet were more susceptible to S. gallinarum. Similar reports indicating the critical role of iron in inducing infection to chicks are also available (Smith et al., 1977a,b; Hary, 1979). Iron is an essential element for growth of pathogenic enteric bacteria including Clostridium botulinum. Elevated iron concentrations in drinking water or the feed had been attributed to intestinal proliferation of C. botulinum and subsequent by the occurrence of botulism (Recelunas et al., 1999).

Stress originating due to over crowding of birds increased mortality rate in chicks inoculated with E. coli, the effect being more severe in terms of mortality when ethylenediamine tetraacetic acid (EDTA) was added in diet (Tufft and Nockels, 1991). Elemental, Cu, Zn and Fe changes namely of in serum and other tissues resulting from EDTA might have predisposed the chicks to a higher mortality rate from E. Coli infection as compared to those of the control birds. Taurine has been known to play important roles in cardiovascular and nervous system. However, its addition in diet at 0 to 0.2% level did not alter resistance or susceptibility of chicks to E. coli infection (Dunnington et al., 1996). Addition of vitamin A in diet of chickens suffering from Mycobacterium tuberculosis improved survival rate by 26% (Solotorovsky et al., 1961). Dietary supplementation with vitamin A or vitamin E reduced E. coli-induced mortality in chickens (Cheville, 1979) and the effect was attributed to increased antibody production and phagocytosis (Tengerdy and Brown, 1977). Supplementation of 150–300 mg vitamin E/kg diet in form of D-a tocopheryl acetate gave increased protection against a relatively moderate mortality in E. coli infection in birds (Heinzerling et al., 1974).

Several feed restriction programmes have been in vogue to control feed intake and thereby improve reproduction in broiler breeders, forced molting and slaughter traits of birds. The chicks shifted from alternate day to the ad lib item feeding were found to be more susceptible to the E. coli infection (Katanbaf et al. 1988). Feed withdrawal i.e. starvation before processing of broiler chickens has also been associated with increased colonization by bacterial enteropathogens. The crop serves as a reservoir for salmonellae in chicks (Hargis et al., 1995) and the feed withdrawal has been linked to an increase in the number of colonized salmonellae in the crop of broilers (Ramirez et al., 1997).

Osteomyelitis outbreaks by Staphylococcus aureus have been found associated with severe feed restriction, poor nutrition, over crowding in turkeys (Mutalib et al., 1983, Zhu and Hester, 2000). 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 (Zhu and Hester, 2000). Similarly, feed restriction is a common programme in raising of broiler breeders and may play an important role in the development of staphylococcal osteomyelitis and synovitis (Page, 1982).

Nutrition and viral infections

The low protein diets (8% CP) or those with excess protein (41 % CP) increased severity of Newcastle disease as indicated clinically and also by the RNA/DNA ratio observed in liver cells (Squibb, 1964). However, growth depression was less with lysine deficient than on control diet, and fatality rate increased in chicks receiving borderline vit. A deficient diet (Squibb, 1961). Similarly, Sijtsma et al. (1989) observed that pre-existing marginal vitamin A status increased the severity (mortality and morbidity) of the disease. Following Newcastle Disease Virus (NDV) infection, the plasma vitamin A level reduced to a level that could be regarded as deficient. Birds receiving 3600 or 10,000 IU of vitamin A/lb of diet experienced greater live weight during active disease condition following infectious bronchitis infection (Panda et al., 1962) but the course of the disease was not altered even when vitamin A concentration was 5 times than the requirement (Gratzl et al., 1963). Pardue (1987) reported that supplementation of vitamin C in diet of chicks increased resistance against infectious bursal disease. The effect of vitamin E deficiency on chick mortality as induced by avian encephalomyelitis (AE) virus was examined (Cheville and Monlux, 1966), the deficient chicks appeared slightly less susceptible than the control chicks.

Nutrition and gut protozoal infections

Although no nutrients are known to act prophylactically against coccidia (Fayer and Reid, 1982), the nutritional status of the host is known to increase as well as decrease the severity of infection. Supplemental vitamin A in diet over normal level did not reduce mortality or morbidity but helped the chicks to recover fast (Reid, 1972). Mortality due to E. tenella and E. necatrix infections was reduced on supplementation of diet with vitamin K but no beneficial effect against non-haemorrhagic species of coccidia e.g., E. acervulina, E. brunetti and E. maxima (Ryley and Hardman, 1978) were observed. Vitamin K @ 0.53 mg/kg diet reduced clotting time and prevented haemorrhage. Colnago et al. (1984) concluded that supplementation of selenium @ 0.25 mg/kg or vitamin E @ 100 mg/kg diet reduced mortality and increased body weight gain of non-immunized chicks infected with E. tennella. The coccidia require many vitamins and metabolites for normal development viz., thiamine, riboflavin, nicotinic acid, biotin, folic acid, panthothenic acid, pyridoxine, retinal, calciferol, ascorbic acid, menadione, choline, inositol, cyanocobalamin, para-amino benzoicacid and glutamic etc. Deficiency of these vitamins or the presence of antimetabolites or vitamin antagonistic elements would interfere with their normal development. Several anticoccidial drugs act by antagonizing vitamins; for example sulphonamides antagonize para-amino-benzoic acid, amprolium is an antimetabolite of thiamin, and pyrimethamine antagonizes folic acid (Fayer and Reid, 1982). Coccidiosis and ascorbic acid @ 150 mg/kg diet interacted to increase feed intake, lower plasma concentration and heterophil; lymphocyte ratios (Mckee and Harrison, 1995).

In groups of chickens fed diets containing 0, 5, 10, 15, 20 or 30% protein before inoculation with oocysts, fatalities increased progressively upto 15% dietary protein (Britton et al., 1964). Eimeria oocysts require trypsin for excystation and releasing of infective sporozoites. A protein deficiency or as little as 48 hours of fasting reduces available trypsin to inconsequential levels and thereby protects the birds. On addition of trypsin to the oocyst inoculum, the antagonism was avoided (Britton et al., 1963; 1964).

Chicks artificially infected with E. tenella and fed 24% protein in diet suffered high mortality than those fed 16 or 20% crude protein. However, in E. acervulina infection higher protein was beneficial to protect weight loss (Sharma et al., 1973). After a natural outbreak of intestinal coccidiosis, a high protein diet seemed more beneficial (Harms et al., 1967). Diet supplemented with 4% fish oil attenuated the growth depressing effect of E. tenella (Korver et al., 1997). Chicks suffering from E. acervulina or mixed coccidiosis responded remarkably with increased gain and improved feed conversion efficiency when excess zinc added to the high calcium (1.82% or 2.00%) diet (Bafundo et al., 1984; Khanagwal et al., 2000a,b). Supplementation of diet with extra calcium and zinc on the face of coccidial outbreak was beneficial in improving feed conversion efficiency (Singh et al., 1997a, b). Dietary level of calcium and or zinc did not alter the course of coccidiosis as oocysts output remained similar. However, mortality was lower at high calcium (1.98%) and high zinc (93 or 123 ppm) containing diet (Khanagwal, 1995; Singh et al., 1997a, b). Supplementation of phosphorus in the form of disodium phosphate did not prove beneficial and rather decreased feed intake due to unpalatability of feed. Aflatoxin in diet of birds increased the severity of E. tenella (Wyatt et al., 1975) and E. acervulina infections (Ruff and Wyatt, 1978). The addition of sodium carbonate in diet at 0.2 to 0.4% level yielded benefits in lesion score and body weight (Hooge et al., 1999). However, the responses of supplemental nutrients are variable depending upon the type of coccidial infection and pathogenesis involved.

Nutrition and immunocompetence

The ability of poultry to withstand infectious disease caused by bacteria, virus or protozoa depends upon the integrity of immune system. The immune system consists of diverse cell populations. Avian cellular immune system consists of rapidly dividing cells (Dietert et al. 1990). The commercial poultry environments harbour different microorganisms, which are challenging the immune system continuously. Proper functioning of the immune system depends upon the availability of nutrients, the precursors for cell growth and activity. Immunity can be impaired by nutrient deficiency and biological amines. Immune stimulation decreases appetite and muscle protein accretion, increases metabolic rate, body temperature, and oxidative damage to cells (Swick, 1995).

Both low and high vitamin A intakes resulted in impaired immune responses (Friedman and Sklan, 1997). Low dietary vitamin A level caused reduced antibody production, defective T-cell responses and reduced phagocytosis, and decreased resistance to infection by bacterial pathogen (E. coli; Friedman et al., 1991), Mycoplasma (Boyd and Edwards, 1962); viral pathogen viz. Newcastle disease virus (Davis and Sell, 1989) and turkey pox (Sklan et al., 1995) and protozoan enteropathogens e.g. coccidia (Singh and Donovan, 1973). Optimum immune responses in growing chicks and poults were observed at 3–10 fold higher dietary vitamin A levels than specified by NRC (Friedman and Sklan, 1997). The retinoids direct differentiation, development and morphogenesis by pre-activated gene amplification in immune response cells (Wolf, 1991; Friedman et al., 1991). Nutritional deficiencies of vitamin E and selenium impaired immune function as measured in terms of humoral response to sheep erythrocytes in young chicks (Marsh et al., 1981). The deficiency of vitamin E and Se in chicks depressed bursa weight, reduced the overall number of lymphocytes found in the primary lymphoid organs and spleen, and resulted in destructive histological changes within these tissues (Marsh et al., 1982). Vitamin E supplementation at higher levels (150–300 IU/kg) increased antibody production against NDV vaccination (Raza et al., 1997). It has been established that immunostimulation effect by vitamin E and Se were related to their antioxidant properties, and that the stimulation of Se was independent of vitamin E nutrition of the host (Colnago et al., 1984).

The possible mechanisms for Se action may have been due to a greater glutathione peroxidase activity which helps to protect membranes of lymphocytes from prooxidants. Selenium may also be involved by modifying the metabolism of arachidonic acid to prostaglandin precursors or related compounds, thus enhancing immune response by reducing endogenous production of prostaglandins because the prostaglandins and related compounds are involved in immune response (Stenson and Parker, 1980; Goodwin and Webb, 1980, Colnago et al., 1984; El Boushy, 1988). Supplemental vitamin C in diet of healthy chicks did not augment antibody production but did so in the immunosuppressed chicks (McCorkle et al., 1980; Pardue et al., 1985). Fasting as practiced in meat-type breeders, increased resistance to deleterious effects of E. coli (O' Sullivan et al., 1991) and E. tenella (Zulkifli et al 1993) infections. Feed restriction enhanced development of endocrine glands and also humoral immunoresponsiveness (Klassing, 1988). Feeding alterations such as imbalance of protein, low energy and dietary fibre impaired immune competence and disease resistance (Scott et al., 1982; Boa-Amponsem et al., 1991). Though, the level of dietary energy alone or energy and protein did not alter antibody titre to sheep RBC or weight of lymphoid organs (bursa and spleen) in commercial broilers (Reddy et al., 1998; Praharaj et al., 1999a), but an interaction existed between genotype and dietary energy level in another experiment (Praharaj et al., 1999b). Broiler chicks fed higher protein in diet (23% CP) revealed better persistency in antibody production to sheep RBC at 10 or 15 days post-injection (Praharaj et al., 1998). However, long-term obesity but not short term weight gain had deleterious consequences for reproductive characteristics, response to sheep RBC antigen, resistance to E. coli and livability (O' Sullivan et al., 1991). Evidences (Tsiagbe et al., 1987; Hall et al., 1986) also existed that methionine is also an essential input for proper functioning of the immune system. Methionine deficiency depressed immune responsiveness. Lymphocytes have also specific methionine requirements. However, important benefits arise from increasing the dietary level beyond a level required for optimum growth.

Certain trace elements like zinc, iron, copper, manganese and selenium are important for normal immune function and disease resistance (Fletcher et al., 1988; Reddy and Frey, 1990). Presence of adequate zinc in the biological system is crucial to normal development, maintenance and functioning of the immune system (Dardenne and Bach, 1993). Zinc is important for proper functioning of heterophils, mononuclear phagocytes and T-lymphocytes (Kidd et al., 1996). As the avian immune system consists of rapidly dividing cells (Dietert et al., 1990), an adequate cellular zinc is crucial for enzyme functions that facilitate their proliferation (Vruwink et al., 1993).

Role of feed additives in disease prevention

Probiotics

Probiotics are the live microbial feed supplements which beneficially affect host animal by improving its microbial balance, nutrition and health. Continuous feeding of probiotics helps in maintaining health by two ways viz. competitive exclusion of pathogens and antagonistic activity towards pathogenic bacteria. Lactic acid bacteria are able to inhibit the growth of Salmonella strains and E. coli (Chateau et al., 1993; Oyarzabal and Conner, 1995; Jin et al., 1996). The administration of Enterncoccus faecium significantly decreased clostridial counts adhering to the crop wall as well as in the caecal content (Kmet et al., 1993). An interaction (competitive exclusion) between Bifidobacteria and Salmonella had also been reported (Famworth et al., 1995). Salmonella colonization was reduced (P < 0.05) but Campylobacter colonization was not affected by yeast treatment (Line et al., 1998). In a field trial, there were significant decrease in the number and detection rate of Campylobacter, detection rate of Salmonella, number of Clostridium perfringens and Enterobacteriaceae and increases in the number of lactobacilli after B. subtilis administration (Maruta et al., 1996). Chicks inoculated with' caecal culture had lesser number of adherent microbes (Salmonella) in the caecal mucosa (Yu et al., 1999). The possible mechanism for antagonistic effect of probiotics has been reviewed by Jin et al. (1997). The antagonistic effect of lactobacilli has been attributed to low pH, low redox potential and the production of inhibitory substances like bacteriocins, organic acids, hydrogen peroxides, etc. The proposed mechanisms for competitive exclusion include aggregation between lactic acid bacteria with pathogens, competition for adhesion sites, competition for nutrients and production of bacteriocidal substances (Jin et al., 1997). Probiotics specialty the lactobacilli and Bacillus cereus are also important in the development of immunocompetence against enteric infections (Perdigon et al., 1995). However, the responses obtained depended upon several factors viz. microbial strain, number of viable cells per unit feed, type and nature of diet, age of birds and sanitary conditions of poultry house.

Prebiotics

Prebiotics are non-digestible feed ingredients that beneficially affect the host by selectively stimulating the growth and/or activity of one or a limited number of bacteria in the colon, that can improve the host health. Galacto-oligosaccharides, fructo-oligosaccharides and lactose derivatives have been used in poultry and other non-ruminants (Peeters et al., 1992; Morisse et al., 1992; Chambers et al., 1997). The oligosaccharides may directly inhibit the growth of certain intestinal pathogenic species by increasing the concentration of lactic acid thereby decreasing pH in the lower gut (Choi et al., 1994; Okumura et al., 1994). Microbes are able to attach themselves to the mucosa through recognition of oligosaccharide binding sites on the wall (Morgan et al., 1992). Dietary oligosaccharides attract microbes away from the intestinal binding sites and, therefore, reduce, colonization by pathogens. Chickens treated with fructo-oligosaccharides had a four-fold, reduction in the level of Salmonella present in caeca (Bailey et al., 1991) and the reduction was attributed to a shift in the intestinal gut microflora. Moreover, certain oligosaccharides like 1,2-gluco-oligosaccharides substrate for beneficial Bifidobacterium spp., at lower tract which favoured their colonization but prevented those of the Clostridium, Enterobacter, E. coli, Enterococcus, etc. (Monsan and Paul, 1995). The effect of dietary lactose and Lactobacillus acidophilus on the colonization of Salmonella enteritidis in newly hatched Leghorn chicks concurrently infected with Eimeria tenella has been studied (Qin et al., 1995). The caecal population of S. enteritidis was increased significnatly by E. tenella infection. Supplementation of lactose alone or the combination of lactose and L. acdiphillus reduced the population of S. enteritidis in the caeca of birds infected with E. tenella but the combination was more effective than lactose alone. Similarly, culture of indigenous caecal bacteria together with dietary lactose controlled S. typhimurium caecal colonization effectively in newly hatched broiler chicks (Corrier et al., 1993, Kogut et al., 1994). However, neither the lactose nor Lactobacillus (or organic acid, egg powder) prevented colonization of S. enteritidis or organ invasion of chicks in another experiment (Opitz et al 1993).

The information provided herein is the clear indicative of close relation between nutrition and the health of poultry and that many of the nutrients have been found to influence the growth, production and reproductive capacity of the birds significantly. The effects have been more clear in the high-producing stocks. Therefore, the managemental practices involving host's nutrition can be a potential component in an integrated approach towards ensuring a sound health and thereby controlling infection, an area which has so far poorly been exploited. Nutritional studies in future should also incorporate immunological aspects along with the traditional growth and production criteria. Because the nutrition also has a direct bearing on outcome of disease in the infected animals, the interaction of infectious diseases with different nutrients along with the optimum level of interacting nutrients need to be established. As the immunoresponsive 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. There is also a need to consider the nutrition, disease control and flock management together to ensure maximum profitability from poultry production.

Top