Effect of dietary plant charcoal from Canarium schweinfurthii Engl. and maize cob on aflatoxin B1 toxicosis in broiler chickens

J R Kana, A Teguia and J Tchoumboue

Department of Animal Productions, Faculty of Agronomy and Agricultural Sciences, University of Dschang, POBox 70 Dschang, Cameroon
kanajean@yahoo.fr

Abstract

A study was conducted to evaluate the effect of including plant charcoal from Canarium schweinfurthii (charcoal A) and maize cob (charcoal B) in the diet on aflatoxin B₁ toxicosis in broiler chickens. Three-weeks-old male chicks (Hybro) were randomly divided into 8 groups of 20 individual birds each individually caged in a completely randomised design. The birds in group 1 received diet C- without aflatoxin B₁ and considered as negative control, while the chickens in group 2 were fed with diet C+ (positive control) containing 22.02 ppb of aflatoxin B₁ produced in peanut meal by Aspergillus flavus. The chickens in groups 3 to 8 were fed diets containing 22.02 ppb of aflatoxin B₁ and supplemented with either 0.20, 0.40, or 0.60% of charcoal A (A_0.20, A_0.40 and A_0.60 respectively) or charcoal B (B_0.20, B_0.40, and B_0.60 respectively).

The result indicated that feeding 0.20, 0.40 and 0.60% of charcoal A and 0.60% of charcoal B significantly (p<0.05) increased feed consumption as compared with C+. Birds fed 0.20, 0.40 and 0.60% of charcoal A had significantly (p<0.05) higher final body weight as compared with C+. When compared with C+, birds fed 0.40 and 0.60% of charcoal B had significantly (p<0.05) higher body weight, average weight gain and intestine length. Feed conversion ratio, intestine circumference, carcass yield, relative weight of legs, heart and abdominal fat were not affected either by aflatoxin B₁ or charcoal. Both charcoal A and B depressed (p<0.05) liver weight and increased intestine density as compared with C+.

It was concluded that 0.20% of Canarium schweinfurthii charcoal and 0.60% of maize charcoal could be used as feed additives to absorb aflatoxin B₁ and promote growth performance of broiler chickens.

Key words: Aspergillus flavus, Feed utilisation, Finisher diet, Growth performance, Mycotoxins

Introduction

Aflatoxins contamination of feeds is a serious problem worldwide resulting either from improper storage or preharvest contamination of maize, peanuts, cotton seed and tree nuts amongst others (Nahm 1995). In Africa, there is ample evidence of the direct and negative effects of aflatoxin on animal production through reduced feed intake, poor growth, gastrointestinal lesions, neurological disturbance, immune suppression and increased incidence on liver functions (Ramos et al 1996, Mabbett 2004).

Aspergillus flavus Link is the saprophytic mould known for its ability to grow on a wide range of organic substrates, alters the nutritional and organoleptic qualities of stored food products (Antonio et al 1996, Mabbett 2004) and it produces aflatoxins and other mycotoxins (Placinta et al 1999). However, various practices including major changes in harvesting methods and storage can have important effects on mould growth and subsequent mycotoxin production. A variety of physical, chemical and biological approaches to reduce the incidence of mycotoxin in feed has been reported (Dalvi and McGowan 1984, Ramos et al 1996, Komkrich 2004), but large-scale, practical and cost-effective methods for a complete detoxification of mycotoxin-containing feedstuffs are currently not available. Amongst the promising mycotoxin binders in animal feed, activated charcoal, a non soluble powder formed by pyrolysis of organic materials has shown to have absorbent properties of a wide variety of drugs and toxic agents (Ramos et al 1996). Activated charcoal has been used to prevent the gastrointestinal absorption and to increase direct elimination of various xenobiotics. In recent years, many synthetics mycotoxin binders have been introduced in the market (Nahm 1995, Ramos et al 1996).

However, the use of these protectants is associated with drawbacks such as toxicity to animal, residues in the meal. Because of these limitations, there is a necessity to investigate the effect of natural, practical, and cost-effective substances as alternative.

The objective of the present study was to investigate the effect of plant charcoal from Canarium schweinfurthii (Photos 1 to 3) and maize cob on aflatoxicosis in broiler chickens.

Material and methods

Diets and experimental design

The experimental birds (males, Hybro) were obtained from a flock of Hybro commercial line (Eurobird, Hendrix Genetics Company) male broiler chicks acquired from a local hatchery and litter-brooded to 21 days of age at a density of 20 birds\m². Aflatoxin B₁ was produced on peanut meal substrate. Five kilograms of peanut meal were soaked in 4 L of water in 10 L bucket overnight. The bucket was autoclaved at 125°C during 15 min, cooled and inoculated with Aspergillus flavus. Then, 1 L of sterile water was added and the bucked was incubated at 20°C for 10 days. After incubation, the moulty peanut meal was steamed at 100°C for 1 h to kill the spores, followed by drying in hot air oven overnight at 60°C. The dried peanut culture was ground to fine powder and analysed for aflatoxin B₁ content using the Enzyme Linked Immuno-Sorbent Assay (ELISA) with Immuno enzymatic kits [(Transia Plate Aflatoxin B₁, PT 53 2004-Rev.4 (IncE:LC95%, K=2)]. After fermentation, the peanut culture obtained containing 116.50 ppb of aflatoxin B₁ was mixed with mycotoxin free ingredients to obtain a final concentration of 22.02 ppb and used as positive the control (C+).

Canarium schweinfurthii seeds (charcoal A) and maize cob (charcoal B) collected in villages around the Experimental Farm were burnt, quenched with water, dried and sieved to pass a 1 mm mesh. The dietary treatments consisted of supplementing the positive (C+) control diet (Table 1) with 0, 0.2, 0.4 or 0.6% charcoal A or charcoal B.

A total of 160 male Hybro birds with a body weight (BW) of 678±50g were individually caged at a density of 0.12m²/bird from 21 to 49 days of age. Each of the 8 experimental diets was fed to ten individual birds, chosen at random in a completely randomized design with 8 treatments replicated 20 times. A test group was fed a diet C- without contaminated peanut meal (negative control).

At 49 days of age, five birds per treatment were randomly selected, fasted for 24 hours, weighed and slaughtered as indicated by Jourdain (1980). The weight of ready to cook carcass, abdominal fat, liver, heart, pancreas, gizzard, head, legs and the weight, length and circumference of the intestine were measured. For the intestine, the cut was done from the start of the duodenal loop to the end of the cloaca. Density of the intestines was calculated as the ratio between the weight and the length of the intestine.

Statistical analysis

All data were subjected to analysis of variance procedures as described by Vilain (1999) and in case of statistical difference, the means were compared using the Duncan’s Multiple Range test. The SPSS computer software package was used for all statistical analysis.

Results 

The effect of feeding diets containing aflatoxin B₁ and graded levels of charcoal A or B on chick performance is presented in Table 2.

When compared with negative control (C-), average feed intake was (P<0.05) lower for the chicks fed diets containing aflatoxin B₁ without charcoal (C+), B_0.20 and B_0.40. When compared with the C+, feed intake was higher (P<0.05) for chicks fed diet A_0.20, A_0.40, B_0.60 and C-. However, there was no difference between C- and groups fed charcoal except B_0.20 and B_0.40 for feed consumption. Birds under the C+ and B_0.20 treatments recorded significantly (P<0.05) lower final body weight as compared to all other treatments. Body weight gain was significantly (P<0.05) higher for birds fed C-, A_0.20, A_0.40, A_0.60 and B_0.60 when compared with C+. When compared with C-, the average weight gain was significantly (P<0.05) lower in birds fed A_0.60, B_0.20, B_0.40 and C+. However, there was no difference among treatments for feed conversion ratio.

The intestine was longer (P<0.05) in birds fed B_0.40 and B_0.60 as compared with all other groups, (Table 3).

No significant (P>0.05) difference was noticed between birds fed A_0.20, A_0.60, B_0.20, C- and C+ for the intestine length. For the intestine circumference, no significant difference was noticed between all treatments. The heaviest intestine was recorded in birds fed diets B_0.20 and B_0.40 as compared with all other groups including C- and C+. When compared with that of birds fed C+, the intestine density of birds from all other groups was significantly (P<0.05) higher. Intestine density was comparable for birds from A_0.40, A_0.60, B_0.20, B_0.40 and B_0.60. When compared with all groups, the intestine density of birds fed A_0.20 was significantly (P<0.05) the highest. The gizzard (g/kg BW) of birds fed A_0.60 was smallest (P<0.05) and that of broiler fed B_0.20 and B_0.60 biggest, when compared with C- and C+. The birds fed A_0.20, A_0.40, B_0.40, C- and C+ had comparable gizzard percentage.

No differences were noted among treatments for carcass, legs, heart and abdominal fat yield (Table 4).

Birds consuming diets A_0.20, A_0.40, A_0.60 and B_0.20 had (P<0.05) smaller head as compared with C- and C+. Feeding 0.40 or 0.60% of charcoal B to birds did not affect the head as compared with C- and C+. C+ increased (P<0.05) the liver weight while both charcoal A and B maintained its proportion unchanged as compared with C-. Feeding A_0.20, B_0.2, B_0.40 or B_0.60 significantly (P<0.05) depressed the pancreas as compared with C-. There was no difference between C-, C+ and A_0.40 for pancreas weight. No significant difference was recorded among treatments for abdominal fat.

Discussion 

Aflatoxins constitute a group of potent mycotoxins, with aflatoxin B₁ being among the most toxic. Depression of feed intake observed in the C+ birds is consistent with previous studies in which chickens were fed diets containing 10 ppm of aflatoxin B₁ (Dalvi and McGowan 1984) or 2.5 ppm of aflatoxin B₁ (Scheideler 1993). The depression in feed intake recorded in chickens fed diet contaminated with 22.02 ppb of aflatoxin B₁ without charcoal or with 0.20% of charcoal B could be associated with gastrointestinal injury caused by this toxin. Robens and Richard (1992) suggested that severe oral lesions in animal, as caused by mycotoxins, impair their ability to eat, thus resulting in reduced BWG. In the present study, the lack of aflatoxin B₁ effect on FCR agree with Jones et al (1982).

The lower BWG in birds fed C+ as compared with C- or the charcoal contains diets confirm previous reports indicating that charcoal reduced toxic injury to the liver (Ademoyero and Dalvi 1983) and improved feed intake and BWG (Dalvi and McGowan 1984). It was postulated that aflatoxin B1 (Bertina 1989, Dalvi and Ademoyero 1984, Ramos et al 1996, Komkrich 2004) and endotoxins produced by intestinal microflora (Cooney 1980, Poppenga et al 1987, Neuvonen and Olkkola 1988, Rotter et al 1989) are absorbed by charcoal, thus becoming unavailable for gastrointestinal absorption.

The intestine was significantly longer in birds fed B_0.40 as compared to other groups. This result contradict the findings of Gunal et al (2006) who reported that supplementing diets with probiotic, antibiotic or organic acids did not improved the development of intestine. The intestine density (weight/length) which is considered as an indicator of the intestinal villi size of the mucosa layer (Abdel-Fattah et al 2008) was increased with charcoal inclusion. This result is consistent with Abdel-Fattah et al (2008) that supplementing diets with organic acids improves intestinal length and intestinal weight. Feeding 0.60% charcoal A to birds decreased gizzard weight.

There was neither the effect of aflatoxin nor that of charcoal on heart, legs and abdominal fat. Both charcoals reduced liver weight as compared with C+ a finding which is in agreement with previous reports on the effect of 200 mg activated charcoal/kg in birds fed a diet containing 6mg of aflatoxin B₁/kg (Ademoyero and Dalvi 1983), with a diet containing 10 mg of aflatoxin B₁ and 1g of activated charcoal/kg (Dalvi and McGowan 1984).

Conclusion 

• From the result of this study, it could be concluded that plant charcoal from 0.20% Canarium charcoal and 0.60% maize charcoal could be used in poultry feed as aflatoxin B₁ binders.

References 

Abdel-Fattah SA, El-Sanhoury M H, El-Mednay N M and Abdel-Azeem F 2008 Thyroid activity, some blood constituents, organs morphology and performance of broiler chicks fed supplemental organic acids. International Journal of Poultry Science 7 (3): 215-222.

Ademoyero A A and Dalvi R R 1983 Efficacy of activated charcoal and other agents in the reduction of hepatotoxic effects of a single dose of aflatoxin B₁ in chickens. Toxicology Letter 16: 153-157.

Antonio J R, Johana F G and Enrique H 1996 Prevention of toxic effects of mycotoxins by means of non-nutritive absorbent compounds. Journal of Food Protection. (59) 6. 631-641.

Betina V 1989 Biological effects of mycotoxins. In: Betina V (editor). Mycotxins: chemical, biological and environmental aspects. Elsevier Science Publishers, Amsterdam. 42-58.

Cooney DO 1980 Activated charcoal: antidotal and ather medical uses. Marcel Dekker, New York. 80p.

Dalvi R R and Ademoyero AA 1984 Toxic effects of aflatoxin B₁ in chickens given feed contaminated with Aspergillus flavus and reduction of the toxicity by activated charcoal and some chemical agents. Avian Diseases 28: 61-69.

Dalvi R R and McGowan C 1984 Experimental induction of chronic aflatoxicosis in chickens by purified aflatoxin B₁ and its reversal by activated charcoal, Phenobarbital and reduced glutathione. Poultry Science 63: 485-491.

Gunal M, Yayli G, Kaya O, Karahan N and Sulak O 2006 The effects of antibiotic growth promoter, probiotic or organic acid supplementation on performance, intestinal microflora and tissue of broilers. International Journal of Poultry Science 5 (2): 149-155.

Jones F T, Hagler W M and Hamilton P B 1982 Association of low levels of aflatoxin in feed with productivity losses in commercial broiler operations. Poultry Science 61: 861-868.

Jourdain R 1980 L’aviculture en milieu tropical. (Editor) Jourdain. International Couloumiers. 43-45.

Komkrich P 2004 Absorption of aflatoxine. Asian Poultry Magazine, June 2004. Pp 1-2.

Mabbett T 2004 The single most serious constraint on poultry production in humid climates. Poultry International 43(12): 38 - 41.

Nahm KH 1995 Possibilities for preventing mycotoxicosis in domestic fowl. World Poultry Science Association. 51. Pp 177-185.

Neuvonen P J and Olkkola K T 1988 Oral activated charcoal in the treatment of intoxications. Role of single and repeated doses. Medicinal Toxicology 3: 33-58.

Placinta C M, D’Mello J P F and Macdonald A M C 1999 A review of worldwide contamination of cereal grains and animal feed with Fusarium mycotoxins. Animal Feed Science and Technology 78. Pp 21-37.

Poppenga R H., Lundeen G R, Beasley V R and Buck W B 1987 The assessment of a general therapeutic protocol for the treatment of acute T-2 toxicosis in swine. Veterinary and Human Toxicology 29: 237-239.

Ramos A J, Fink-Gremmels J and Hernandez E 1996 Prevention of toxic effects of mycotoxins by means of non-nutritive absorbent compounds. Journal of Food Protection 59 (6): 631-641.

Robens J F and Richard J L 1992 Aflatoxins in animal and human health. Revue of Environment Contamination and Toxicology 127: 69-94.

Rotter R G, Frohlich A A and Marquardt R R 1989 Influence of dietary charcoal on ochratoxin A toxicity in Leghorn chicks. Canadian Journal of Veterinarian Research 53: 449-453.

Scheideler S E 1993 Effects of various types of aluminosilcates and aflatoxin toxicity, chick performance, and mineral status. Poultry Science 72: 282-288.

Vilain M 1999 Méthodes expérimentales en Agronomie. Pratique et analyse. Editions Tec et Doc. Paris. 337p.

Received 29 December 2009; Accepted 19 February 2010; Published 1 April 2010

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