Poultry

 

 

All poultry species are affected by mycotoxins. However, species differences have been reported; ducks for example are particularly sensitive towards aflatoxin. In poultry production, feed is the key vector for introducing mycotoxins into flocks and control strategies should, therefore, focus on optimising feed quality. Other routes of exposure include litter. Chopped straw litter may be contaminated with significant concentrations of mycotoxins at the time of harvest, although any type of litter can be contaminated if kept under unfavourable storage conditions.

In order to effectively recognise mycotoxicosis, flocks need to be carefully inspected for clinical signs. Symptoms can be very general and vary greatly between mycotoxins, making proper diagnoses a difficult undertaking. Careful monitoring, recognition of symptoms and post-mortem analyses combined with adequate feed analyses provides the most accurate mean of a mycotoxicosis diagnosis within large flocks of poultry.

 

 

Symptoms of mycotoxicosis

 

Common symptoms of mycotoxicosis in poultry include:

• Reduced feed consumption
• Poor growth
• Reduced egg production
• Reduced feed conversion efficiency
• Increased susceptibility to diseases
• Increased mortality
• Poor egg shell quality
• Reduced fertility
• Leg problems
• Carcass condemnation

 

Aflatoxins

Aflatoxins commonly occur in feed materials grown in warm and humid climatic conditions. It is generally considered as a storage mycotoxin. However, it can be produced in the field especially during draught conditions. Although aflatoxins are not considered to be a major problem in cold or more temperate regions, caution must be exercised in colder climates when using feedstuffs imported from warm and humid regions.

Among poultry, ducks are the most susceptible to aflatoxins, followed by turkeys, broilers, laying hens and quail. In all species, aflatoxins are hepatotoxic, causing fatty livers, hepatocyte degeneration, necrosis, and altered liver function. Suppression of hepatic protein synthesis causes growth suppression and reduced egg production. Aflatoxins negatively affect lipid and pigment digestion by reducing bile salt production,.

Aflatoxin is known to interfere with vitamin D metabolism, contributing to reduced bone strength and leg weakness, which may exacerbate existing problems. Trials with aflatoxins have shown increased incidence of rickets in affected flocks. Interferences with Ca deposition in bone has been demonstrated as reduced tibial ash (Raju and Devegowda, 2000), and levels of 1 ppm can affect circulating P and Ca levels (Eraslan et al., 2005). Leg deformities are particularly pronounced in ducklings (Bintvihok, 2001). Additionally the metabolism of other minerals including iron, phosphorus and copper are affected.
Aflatoxin increases the fragility of capillaries, reduces prothrombin levels and subsequently increases the incidence of bruising in carcasses, leading to downgrading at slaughter (Tung et al., 1971). Due to the transfer of aflatoxin into edible products and its carcinogenic effects in all species including humans, many countries have set upper legal limits for aflatoxin in feed to limit its transmission within the food chain. However, research conducted in Costa Rica (Marin and Villalobos-Salazar, 2009) into the levels expressed in tissues from birds consuming aflatoxin contaminated feed only found the toxin in 12.5% of liver cells, which was at levels of up to 2.5 ppb, well below the 35 ppb limits set locally for human food.

 

Clinical signs of aflatoxin toxicity in poultry include:

• Decreased weight gain/anorexia
• Decreased egg production
• Reduce feed conversion efficiency
• Increased mortality
• Immune suppression and increased disease susceptibility
• Reduced fertility and hatchability
• Embryo toxicity
• Specific visceral haemorrhage
• Increased susceptibility to environmental and microbial stressors
• Leg weakness and reduced bone strength
• ‘Pale bird’ syndrome
• Fatty liver
• Liver necrosis
• Bile duct hyperplasia
• Increased incidence of bruising and downgrading

 

 

Cyclopiazonic acid

 

This mycotoxin is the mina one associated with ‘Turkey X’ disease and is thought to cause the classic symptoms of the drawn back head, stretched out legs and arching of the neck. CPA is known to affect shell strength in laying hens, and so may also interfere with bone structure and maintenance. There is data showing problems with cracked or shell-less eggs from hens affected by CPA, especially at levels around 2.5 mg/kg body weight (Bryden, 1991, Suksupath, 1993). Currently, it is considered that CPA may influence leg strength by inducing fatigue and exhaustion in skeletal muscles and changing the Ca profile of bone (Devegowda and Ravikran, 2009).

 

 

Ochratoxins

 

Ochratoxins are important toxins generated when feedstuffs are poorly stored. They are produced by different fungi and are found in temperate as well as in tropical regions, with ochratoxin A being the most important. The primary effect of ochratoxin A in all poultry species is kidney damage (nephrotoxicity). In poultry the proximal tubules are damaged, and the kidney is pale and grossly enlarged. As with aflatoxin, fatty liver can occur with ochratoxin exposure. In acute cases mortalities can occur due to acute renal failure. In young chicks, ochratoxin A is approximately three times more toxic than aflatoxin.

Ochratoxin has been implicated in significant field outbreaks of mycotoxicosis in poultry. Raju and Devegowda (2000) reported reduced tibial bone ash in broilers fed 2 mg/kg ochratoxin in feed, which may be due to changes induced in protein, enzymes, Ca and P serum concentrations by this mycotoxin. It has also been implicated in problems with egg laying (Devegowda and Ravikran, 2008). Recent investigations with laying hens suggest that ochratoxin in bile, collected directly from the gall bladder, can be used as a bio-marker to identify affected flocks (Mariotti, 2009).

 

Clinical signs of ochratoxin exposure in poultry include:

• Reduced feed intake
• Reduced growth rate and egg production
• Reduced feed conversion efficiency
• Mortality due to acute renal failure
• Poor egg shell quality and higher incidence of eggs with blood spots
• Reduced embryo viability and decreased hatchability
• Reduced feathering
• Weak bones
• Polyurea and large volumes of wet faeces
• Pale and grossly enlarged kidney
• Fatty liver
• Urate deposition in joints and abdominal cavity (at high exposure levels)
• Depletion of lymphocytes and with it strong suppression of cellular immunity, thus enhanced susceptibility to viral infections.

 

 

Trichothecens Mycotoxins

 

Trichothecene mycotoxins: T-2 toxin, diaceptoxyscripenol (DAS), HT-2 toxin,deoxynivalenol (DON), Nivalenol

Trichothecenes are typical field mycotoxins and are produced on crops that are used in poultry feed formulations. There are two types of trichothecene mycotoxins; Type A and Type B. There are more than 100 trichothecene mycotoxins that are known as on today. T-2 toxin, HT-2 toxin and DAS are the predominant Type A trichothecenes whereas DON and Nivalenol are the predominant Type B trichothecenes. Trichothecenes are irritants with the major observation associated with their ingestion are oral lesions, dermatitis and intestinal irritation. The major physiological response to trichothecenes mycotoxins is loss of appetite, thus earning them the common name ‘feed refusal’ toxins.

Poultry is more sensitive to Type A than B but the occurrence of type A in poultry feed is lower than than Type B. DON is considered as a marker for Fusarium mycotoxins because of its occurrence at high levels throughout the world. Trichothecenes are strong immune suppressive agents, affecting cellular immune response by having a direct impact on bone marrow, the spleen, lymphoid tissues, thymus and intestinal mucosa,

 

Clinical signs of trichothecenes toxicity in poultry include:

1. Oral lesions: circumscribed proliferate yellow caseous plaques occurring at the margin of the beak, mucosa of the hard palate and the angle between the mouth and the tongue.
2. Reduced feed intake
3. Reduced weight gain and egg production
4. Poor shell quality and increased breakage
5. Reduced female fertility and hatchability of fertile eggs
6. Immune suppression, reduced vaccination response
7. Tibial dyschondroplasia
8. Gizzard erosion
9. Necrosis of proventricular mucosa
10. Regression of ovaries
11. Increased liver weight

Lesions of the beak



Lesions in the mouth

 

 

Fumonisins

 

Broilers and turkeys seem relatively resistant to acute effects from fumonisins. Ingestion of the toxin leads to a very specific increase in sphiganine:sphingosine ratio, which may be used as a marker of contamination. Research has shown that feeding contaminated feed with levels of up to 200 mg/kg fumonisin B1 (FB1) leads to the development of tibial dyschondroplasia in growing turkey poults (Weibking et al., 1993). This may be due to poorer mineral uptake due to increased diarrhoea in birds affected by FB1 toxicity. However, other work has shown the FB1 can also directly impair the viability of bone cells (chondrocytes) (Chu et al., 1995).

 

Clinical signs of fumonisin toxicity include:

• Spiking mortality
• Tibial dyschondroplasia
• Paralysis
• Extended legs and neck
• Wobbly gait
• Gasping
• Reduced growth rate
• Increased organ weights
• Hepatocellular hyperplasia
• Poor vaccination response
• Increased liver sphinganine:sphingosine ration (biomarker)

Fusarochromanone (FCH)

 This toxin is known to cause skeletal abnormalities in poultry – especially growing broilers (Devegowda and Ravikran, 2009). It appears that the incidence of tibial dyschondroplasia increases in a linear manner according to the levels of FCH in the diet (Wu et al., 1993), where dietary levels exceed 20 mg/kg. However, there are differences between breeds, with some being more affected than others.

 

Clinical symptoms of Fusarium toxin exposure include:

• Tibial dyschondroplasia
• Reduced immunological response
• Reduced feed intake
• Changes in immune responses
• Reduced weight gain
• Reduced egg shell thickness
• Lower eggs mass
• Loss of laying performance and efficiency

 

 

Multiple Contamination

 

Contaminated feeds or ingredients typically contain several mycotoxins. The toxic responses and clinical signs observed in poultry when more than one mycotoxin is present in feed are complex and diverse, and multiple contamination appears to exert greater negative effects on health and productivity than single mycotoxin exposure. For this reason, symptoms typical of mycotoxicosis are often seen in poultry despite analyses of the feed indicating only very low or zero concentrations of individual mycotoxins. Toxicity may be due to interactions between different mycotoxins that exaggerate the toxicity symptoms.

With mycotoxins the risk directly depends on the level of the major mycotoxins in the feed, the co-occurrence and level of other mycotoxins as well as the avian species, their age and health status. Therefore strictly speaking it is not possible to define safe levels of mycotoxins. This complex situation makes it critical to take the necessary precautions.

There are many studies conducted, especially on Fusarium mycotoxins, feeding poultry grains/feed contaminated with multiple mycotoxins. Research conducted with feeds contaminated with more than one type of toxin (Swamy and Reddy, 2009) have shown that broiler chickens have significantly poorer weight gains and feed conversion ratios, especially in the younger birds (up to three weeks of age). Even in diets with no discernable contamination, trials have demonstrated significant benefits in poultry performance with the inclusion of a proven binding agent such as Mycosorb™. Radu-Rusu et al., (2008) showed that, when apparently non-contaminated layer diets were supplemented with Mycosorb™, significant improvements in shell percentage and shell index were observed. Trials run by Swamy et al., (2008), using layers exposed to high levels of various mycotoxins from poor quality Indian feed ingredients, demonstrated that egg production can be progressively recovered back to expected commercial levels from a three-fold lower level of production, when using Mycosorb™ in the feed to bind the toxins.

Research with feed materials naturally contaminated with Fusarium mycotoxins (Girish et al., 2008) demonstrated that turkeys aged  from 21 d and exposed to the infected diet had significantly poorer weight gains between d 28-42 (p=0.02) and d 42-63 (P=0.01) of age, reduced total lymphocyte counts (P=0.03), increased CD4+ lymphocyte levels and decreased CD8+ mediated hyper-sensitivity reaction. Bursal weights were significantly increased (P=0.03) in the treatment group. These effects were mitigated by inclusion of the adsorbent Mycosorb™ in the contaminated diet.

 

Effect of Fusarium contaminated feed on growing turkeys (Girish et al., 2008)

 

Parameter	Control	Fusarium	Fusarium + Mycosorb	P Value
Body weight gain d 28-42 (kg)	1.755a	1.604b	1.761a	0.02
Body weight gain d 43-63 (kg)	2.750a	2.570b	2.713a	0.01
Bursal weight (g)	5.6b	6.6a	5.7b	0.03
Total lymphocytes (109/l) 21-27 d	10.37a	3.81b	8.51a	0.03
CD4+ lymphocytes (%) (d 42)	28.7b	52.6a	34.6b	0.03
24 h hypersensitivity response (as webfoot thickness)	49.0a	20.8b	41.2a	0.02

 

Further work by Girish  et al. (2008) investigated the impact of Fusarium mycotoxins on turkey brain neurochemistry, and found that serotonin levels were decreased in birds fed the contaminated diets. As these compounds regulate feeding patterns in poultry, this may be why mycotoxins affect feed intake.

Laying hens receiving diets contaminated with Fusarium mycotoxins have been shown to have reduced feed intakes in the four weeks of the trial period, and poorer FCR for the remaining eight weeks of the trial (Chowdhury et al., 2004). Egg production was significantly reduced (P=0.0002) from 95% to 81% after four weeks of receiving the contaminated feed, and remained significantly lower until week 8, as did the incidence of lower egg mass.

Feeding broiler breeders with feed contaminated with Fusarium toxins leads to decreased shell thickness and increased early embryo mortality (Yegani et al., 2008). Trials with broiler breeder pullets infected with coccidiosis and exposed to Fusarium contaminated feed revealed that the presence of these mycotoxins caused problems in gut functionality, with significantly reduced apparent villus surface area in duodenum. There was evidence that other areas of the gut developed a larger surface area to compensate for this problem (Girgis et al., 2010a). The research from this same group has shown that the presence of DON and other Fusarium mycotoxins delay immune response to coccidiosis (Girgis et al., 2010b).