Confounding of Brucellosis and Blue Tongue in Trans Humane Sheep Flock of Tamilnadu and other Herd Health Impact_Lupine Publishers

Journal of Veterinary Science| Lupine Publishers

Abstract

This present study was carried out to assess the prevalence of brucellosis and blue tongue in a trans humane sheep flock of Tamil Nadu, India. This Sheep flock had a history of inconsistent abortion, repeat breeder, poor fertility rate and higher prevalence of still birth. Serum samples were collected from sheep by random sampling. Serum samples were subjected to Rose Bengal Plate agglutination test (RBT) and ELISA. The risk factors like pregnancy, abortion, age and sex were correlated to the Brucella seropositivity. This study also assessed for the presence of Bluetongue in aborted sheep. It was found that ELISA could be the choice of test for testing of Brucellosis (with the percentage of 57.14). Clinically healthy rams were found to be with brucellosis seropositivity and posed infertility to ewes. It was observed that in trans humane flocks. Brucellosis and Blue tongue has a confounding phenomenon for ovine abortions.
Keywords: Sheep; Trans Humane; Inconsistent Abortion; Brucellosis; Blue Tongue; Confounding

Introduction

Brucellosis is a bacterial zoonosis caused by microorganisms belonging to Brucella, a genus of gram-negative bacteria that behave as facultative intracellular pathogens of ruminants, suidae, canids, and several wildlife species (OIE, 2008). B melitensis is the foremost etiological agent of brucellosis in sheep and goats. It is also the main agent responsible for human brucellosis known as Malta fever. Abortion and infertility are the predominant clinical signs in small ruminants. B. melitensis infection in sheep and goats has been neglected for long time, because small ruminant production was considered as a represents generally low-income activity practiced by landless farmers and marginalized communities in the developing countries. For these reasons the trans humane farming systems continue to have served disease challenges and pose major hurdles in, the control and eradication of many infections. The reasons for such high prevalence may also be result of socio cultural factors, which were compounded by the lack of adequate control measures being applied in small ruminant production systems as per the observations of WHO [1]. The Rose Bengal Plate Agglutinations Test (RBT) was developed originally for the diagnosis of bovine brucellosis and despite a scant information on its usage for Sheep and Goat is available, it is also recommended for the screening of B. melitensis infection in small ruminants [2]. In general, indirect ELISA was considered good test for surveillance purposes in which vaccination is no longer used [3]. Infected nonpregnant livestock may not demonstrate clinical signs of infection and this makes the control and prevention more challenging [4]. Bluetongue, which is caused by the Bluetongue virus (BTV) and transmitted by Culicoides spp. Midges, is a major infectious disease of sheep [5,6]. Among the economic losses resulting from BTV infection are abortion and those due to congenital deformities such as hydranencephaly and cerebellar aplasia in calves and lambs [7]. BTV serotypes -10, 11, 13 and 17 are able to cross the placenta and cause fetal infection [8]. Limited information on concurrent Brucellosis and Blue tongue in Sheep, especially trans humane flocks are available. This study investigated and documented it in a trans humane Sheep flock of Tamil Nadu.

Materials and Methods

Study Area and Flock Details

This study was carried out during the period between November 2015 to November 2016 in the Cavery delta districts of Tamil nadu, India. These delta districts are the rice bowl of Tamil nadu state and accounts for 75% of the state’s rice production. The rice harvesting season attracts the several Sheep shepherds to this area to graze the paddy fields after harvesting. Trans humane sheep flocks having flock strength ranging from 300 to 5000 animals per ownership are common sights in these areas. Each flock may have about 300 sheep 25 goat and 9 cattle (Figure 1). These animals were not immunized against brucellosis and blue tongue and no periodical deworming programs are followed. In fact no organized animal health care is being practiced by such nomadic farmers.

Figure 1: Trans human Sheep flock with shepherd in delta districts of Tamilnadu.

Choice of Samples

Samples were collected from pregnant non aborted, pregnant aborted, non pregnant ewes and rams. For sample size calculation, expected prevalence of brucellosis was assumed as 20 percent with five percent absolute frequency.

Sampling Methods

Clinical materials like whole blood in EDTA tubes, serum collected in clot activator tubes aseptically and stored in refrigeration until further processing. Simple random sampling method was used for sampling.

Brucellosis Screening

Clinical samples like serum samples were collected and submitted for Brucellosis, Blue tongue, Chalymidiasis, Malignant catarrahal fever and Bovine viral diarrhoea diseases since the season and clinical history had given clues for such pathogens. Rose Bengal plate agglutination test (RBT) and I ELISA tests undertaken for brucellosis identification.

Blue Tongue Screening

For blue tongue identification, whole blood in EDTA was collected and subjected to polymerase chain reaction.

Bovine Viral Diarrhoea (BVD) Malignant Cattarhal Fever (MCF) and Chalymidiasis Screening

Serum samples were collected aseptically and analyzed by nested PCR for BVD and MCF. Serology was carried out for Chalymidiasis.

Test Protocols

Rose Bengal plate agglutination (RBT) was carried out as per the OIE prescribed procedure. The recommended steps to improve sensitivity of RBT by using three volumes of serum and one volume of antigen (e.g. 75μl and 25μl, respectively) in place of an equal volume of each (Figure 2) This was used in this study modification helped in increasing RBT sensitivity and minimized the discrepancies between RBT and other diagnostic tests. Positive serum and antigen purchased from Indian Veterinary Research Institute (IVRI), Bareilly, India was used in this study. Monoclonal based blocking ELISA for diagnosis of brucellosis was adopted as per the manufactures protocol. For Blue tongue Polymerase chain reaction was adopted as per the standard procedure of OIE.

Figure 2: Modified Rose Bengal plate Agglutination Test.

Results

The trans humane sheep population had a clinical history of inconsistent abortion, pooer birth weight of lambs and higher mortality among lambs. Upon screening of 28 clinical samples 15 samples were confirmed as blue tongue with percentage positivity of 53.57. For Brucellosis, out of 10 (35.71%) animals tested by RBT and 16 animals tested by I ELISA (57.14%) were positive for Brucellosis. Out of 12 pregnant aborted animals studied 8 (66.66%) were positive for blue tongue and 7 (58.33%) were shown positive for brucellosis (Table 1) In pregnant non aborted animals, out of the six animals studied three were positive for blue tongue and none of these were positive for brucellosis. Out of five bucks screened, one was positive for blue tongue and two were positive for brucellosis. In non pregnant non aborted animals three and one animals were positive for blue tongue and brucellosis respectively (Table 2). None of the animals were positive for malignant catarrhal fever, Chalymidiasis and Bovine viral diarrhea.

Table 1: Comparison of RBT with ELISA.

Table 2: Comparison of RBT with ELISA.

Discussion

Brucellosis and its mode of transmission were known for over 100 years still, the disease remains inconsistent pandemic, predominantly in developing countries. This study analyzed the cause for in consistent abortion in trans- humane sheep flocks of delta regions of Tamil nadu, India. These sheep flocks were nomadic in nature and following flock matting system. They used to exchange their breeding rams with each other over the period of time. The results of the study indicated that 53.57 % of animals were positive for blue tongue and 57.14% were having antibodies for brucellosis which underscored that the incidence was quiet high. Many previous studies had documented it and had an increasing trend [9,10]. The results from this study indicated that brucella antibodies are widely distributed throughout the flock. Since the flock was not immunized in their life time, presence of antibodies directly correlated to the active infection. Prevalence seems to be higher than the overall country seropositivity (13.5%) in Sheep [11-13]. Indirect ELISA showed higher positivity (57.14%) than RBT (35.71%) which indirectly revealed the sensitivity of these tests (Table 3). More over Monoclonal based blocking ELISA for brucellosis detects the antibodies with traces and LPS coated on the ELISA plate has highly homology of the field variant and showed higher titer value (Figures 2 & 3) Conventional Rose Bengal plate agglutination test detects only IgM and is less sensitive, where as ELISA detects both IgM and IgG antibodies which attracts higher sensitivity [2]. Inconsistent abortion was recorded in this flock indicated that it could be the “chronic Brucellosis form”. Rams played vital roles in the transmission of Brucellosis here since higher number (60%) of them showed seropositivity for brucellosis.

Table 3: Categorization of screening tests and positive for Brucellosis and Blue tongue.

Figure 3: Higher Brucella IELISA titre of Sheep samples.

In India mostly the sero positive animals were handled based on “test and separate” policy rather than the “test and slaughter” policy due to economic concerns of these marginalized nomadic people. Unplanned immunization program coupled with no effective quarantine and uncontrolled trans-state migration of animals are major factors that affects the Brucellosis control programs [9]. Host susceptibility is also variable with the reproductive status. Thus in the field level, all intermediate stages between typical acute infection to complete resistance may be observed. Under pregnant aborted animals category 58.3% and 66.66% animals showed positivity for Brucellosis and Bluetongue respectively and this highlighted that there is certain confounding effect which makes the animal to abort. In pregnant non aborted category lower percentage of animals showed positive for both Brucellosis and Bluetongue which further supports the possibilities of confounding phenomenon augmenting abortion feature. Interesting by aborted animals got pregnant in their next season and gave birth to normal lambs possibly many animals may develop self limiting infections or they become asymptomatic latent carriers and turn in to potential source of future infections. Abortion generally does not occur if the female is infected at the last stage of pregnancy. Non pregnant non aborted animals showed higher Blue tongue positivity than brucellosis which enlightenend the real risk factor for abortion. Non-pregnant animals exposed to small numbers of organisms may develop selflimiting, immunizing infections or they may become latent carriers [12,13]. No proper selection of breeding ram between flocks of Sheep, low /no biosecurity measures, poor awareness about the vaccination had resulted in brucellosis becoming a continuous threat to the trans humane Sheep populations. As 60 % of rams, showed seropositivity for brucellosis, they posed a great threat to the breeding ewes. Interestingly non of the rams showed clinical signs of Brucellosis. Asymptomatically infected rams deserve to have poor fertility and contributes to dissemination of B. ovis and when very high percentage of rams were infected marked infertility becomes evident in the flock [14]. Seroconversion and shedding of bacteria in the semen of infected rams demonstrated mild or no detectable lesions during the acute phase of infection [15].

The study period of October month had a higher culicids’ populations and it in turn would have helped in transmission of Blue tongue. Results here indicated that BTV is epidemiologically important, and further studies are required to determine the true spatial distribution and cause for abortion in Sheep. Unplanned and uncontrolled grazing and frequent addition of flocks of sheep also contribute to the wide distribution of brucellosis in these animals. Even though the goat and cattle reared along with sheep flock, they were not part of this study, however they may had also acted as a cofounder for Brucellosis. Future studies on these aspects will add more information.

To know more about our Veterinary Sciences click on https://lupinepublishers.com/dairy-veterinary-science-journal

To know more about Lupine Publishers click on https://lupinepublishers.us/

To know more about Open access publishers click on Lupine Publishers

Occurance of Mycotoxins and Mycotoxicosis in Poultry_Lupine Publishers

Journal of veterinary science| Lupine Publishers

Opinion

Mycotoxins are biologically active, toxic metabolites produced by toxigenic fungi mainly belonging to Aspergillus, Fusarium and Penicillium species, which invade crops in the field and may grow on feedstuffs during storage under favourable conditions of temperature and humidity [1]. FAO estimated that about 25% of food and feedstuffs are contaminated with mycotoxins and strong efforts have been made to decontaminate them by the use of physical and chemical adsorbents but the success made so far is limited [2]. Like other environmental pollutants, mycotoxins also adversely affect the health and productivity in animals and esecially in poultry [3,4]. The economy of poultry industry is heavily affected due to wide mycotoxin exposure or contamination of various agricultural commodities. The economic losses are primarily due to the decreased growth rate, feed conversion efficacy, carcass yield, carcass quality and increased susceptibility to other diseases caused due to their immunosuppressive effects among the affected poultry. A mycotoxicosis is a disease caused by a natural toxin produced by a fungus. In poultry, this usually results when toxin producing fungi grow in grain and feed. Hundreds of mycotoxins have been identified, and many are pathogenic. Mycotoxins may have additive or synergistic effects with other natural toxins, infectious agents, and nutritional deficiencies. Many are chemically stable and maintain toxicity over time. Out of more than 350 mycotoxins identified in nature, aflatoxins, T-2 toxin, diacetoxyscirpenol, vomitoxin, zearalenone, ochratoxins, ergot alkaloids, oosporein, cyclopiazonic acid, and tricothecenes are the most common and important in poultry [5].

Mycotoxicosis and Their Effect in Poultry

Aflatoxicosis: The aflatoxins are toxic and carcinogenic metabolites such as Aspergillus flavus. Aflatoxicosis in poultry primarily affects the liver but can involve immunologic, digestive, and hematopoietic functions. Aflatoxin can adversely affect weight gain, feed intake, feed conversion ratio, pigmentation, carcass yield, egg production, male and female fertility, and large hatchability problems. Some effects are directly attributable to toxins, whereas others are indirect, such as reduced feed intake. Susceptibility to aflatoxins varies, but in general, ducklings, turkeys, and pheasants are susceptible, while chickens and Japanese quail are relatively resistant. Clinical signs vary from general unthriftiness to high morbidity and mortality. At necropsy the lesions are found mainly in the liver, which can be due to necrosis and congestion or yellow due to lipid accumulation. Hemorrhages may occur in liver and other tissues. In chronic aflatoxicosis, the liver becomes yellow to gray and atrophied.
Fusariotoxicosis: The genus Fusarium produces many mycotoxins injurious to poultry. The trichothecene mycotoxins produce caustic and radiomimetic patterns of disease exemplified by T-2 toxin and diacetoxyscirpenol (DAS). Deoxynivalenol (vomitoxin, DON) and zearalenone are common trichothecene mycotoxins that are relatively nontoxic for poultry but may cause disease in large concetratin in feed. Fusariotoxicosis in poultry caused by the trichothecenes results in feed refusal, caustic injury of the oral mucosa and areas of the skin in contact with the mold,acute digestive disease, and injury to the bone marrow and immune system [3]. Lesions include necrosis and ulceration of the oral mucosa, gastro intestinal mucosa, mottling of the liver, atrophy of the spleen and other lymphoid organs, and visceral hemorrhages. In laying hens, decreased egg production can be accompanied by depression, recumbency, feed refusal, and cyanosis evident in the comb and wattles [6]. Other Fusarium mycotoxins cause defective growth of long bones.
Ochratoxicosis: Ochratoxins are quite toxic to poultry. These nephrotoxins are produced chiefly by Penicillium viridicatum and Aspergillus ochraceus in grains and feed. Ochratoxicosis causes primarily renal disease but also affects the liver, immune system, and bone marrow. Severe intoxication causes reduced spontaneous activity, huddling, hypothermia, diarrhea, rapid weight loss, and death. Moderate intoxication impairs weight gain, feed conversion ratio, pigmentation, carcass yield, egg production, fertility, and hatchability [5, 6].
Ergotism: Toxic ergot alkaloids are produced by Claviceps spp, which are fungi that attack cereal grains. The mycotoxins form in the sclerotium, a visible, hard, dark mass of mycelium that displaces the grain tissue. Within the sclerotium are the ergot alkaloids, which affect the nervous system, causing convulsive and sensory neurologic disorders, the vascular system, causing vasoconstriction and gangrene of the extremities and the endocrine system, including neuroendocrine control of the anterior pituitary gland. In chicks, the toes become discolored due to vasoconstriction and ischemia. In older poultry, vasoconstriction affects the comb, wattles, face, and eyelids, which become atrophied and disfigured. Vesicles and ulcers develop on the shanks of the legs and on the tops and sides of the toes. In laying hens, feed consumption and egg production are reduced [6].

Mycotoxicosis Diagnosis in Poultry

Mycotoxicosis should be suspected when the history, signs, and lesions are suggestive of feed intoxication, and especially when moldy ingredients or feed are evident. Toxin exposure associated with consumption of a new batch of feed may result in subclinical or transient disease. Chronic or intermittent exposure can occur in regions where grain and feed ingredients are of poor quality or when feed storage is substandard or prolonged. Impaired production can be a clue to a mycotoxin problem, as can improvement because of correction of feed management deficiencies. Definitive diagnosis involves detection and quantitation of the specific toxins. This can be difficult because of the rapid and high volume use of feed and ingredients in poultry operations. Diagnostic laboratories differ in their respective capabilities to test for mycotoxins and should be contacted before sending samples. Feed and also poultry that are showing sings of sicknes or recently dead should be submitted for pathological examinatios. A necropsy and related diagnostic tests should accompany feed analysis if mycotoxicosis is suspected. Concurrent diseases can adversely affect production and should be considered. Sometimes, a mycotoxicosis is suspected but not confirmed by feed analysis. In these situations, a complete laboratory evaluation can exclude other significant diseases. Feed and ingredient samples should be properly collected and promptly submitted for analysis. Mycotoxin formation can be localized in a batch of feed or grain. Multiple samples taken from different sites increase the likelihood of confirming a mycotoxin formation zone. Samples should be collected at sites of ingredient storage, feed manufacture and transport, feed bins, and feeders [5, 6].

Prevention of Mycotoxicosis in Poultry

Prevention of mycotoxicoses should focus on using feed and ingredients free of mycotoxins and on management practices that prevent mold growth and mycotoxin formation during feed transport and storage. Regular inspection of feed storage and feeding systems can identify flow problems, which allow residual feed and enhance fungal activity and mycotoxin formation. Mycotoxins can form in decayed, crusted feed in feeders, feed mills, and storage bins, cleaning and correcting the problem can have immediate benefits. Temperature extremes cause moisture condensation and migration in bins and promote mycotoxin formation. Ventilation of poultry houses to avoid high relative humidity also decreases the moisture available for fungal growth and toxin formation in the feed. Antifungal agents added to feeds to prevent fungal growth have no effect on toxin already formed but may be cost effective in conjunction with other feed management practices [6]. Propionic acid are effective inhibitor, but the effectiveness may be reduced by the particle size of feed ingredients and the buffering effect of certain ingredients. Sorbent compounds such as hydrated sodium calcium aluminosilicate effectively bind and prevent absorption of aflatoxin. Esterified glucomannan, derived from the cell wall of the yeast Saccharomyces cerevisiae, is protective against aflatoxin B1 and ochratoxins. It reduces toxicity through the binding and reduction in bioavailability of fumonisins, zearalenone, and T-2 toxin. Various other fermentation products, algae and plant extracts, and microbial feed additives have demonstrated ability to bind or degrade mycotoxins and may be applicable and appropriate for the situation.

Acknowledgement

The paper is a part of the research work on the project III 46012 financed by the Ministry of Education, Science and Technological Development of the Republic of Serbia.

To know more about our Veterinary Sciences click on https://lupinepublishers.com/dairy-veterinary-science-journal

To know more about Lupine Publishers click on https://lupinepublishers.us/

To know more about Open access publishers click on Lupine Publishers

Occurance of Mycotoxins and Mycotoxicosis in Poultry| Lupine Publishers

Dairy and Veterinary Sciences| Lupine Publishers

Opinion

Mycotoxins are biologically active, toxic metabolites produced by toxigenic fungi mainly belonging to Aspergillus, Fusarium and Penicillium species, which invade crops in the field and may grow on feedstuffs during storage under favourable conditions of temperature and humidity [1]. FAO estimated that about 25% of food and feedstuffs are contaminated with mycotoxins and strong efforts have been made to decontaminate them by the use of physical and chemical adsorbents but the success made so far is limited [2]. Like other environmental pollutants, mycotoxins also adversely affect the health and productivity in animals and esecially in poultry [3,4]. The economy of poultry industry is heavily affected due to wide mycotoxin exposure or contamination of various agricultural commodities. The economic losses are primarily due to the decreased growth rate, feed conversion efficacy, carcass yield, carcass quality and increased susceptibility to other diseases caused due to their immunosuppressive effects among the affected poultry. A mycotoxicosis is a disease caused by a natural toxin produced by a fungus. In poultry, this usually results when toxin producing fungi grow in grain and feed. Hundreds of mycotoxins have been identified, and many are pathogenic. Mycotoxins may have additive or synergistic effects with other natural toxins, infectious agents, and nutritional deficiencies. Many are chemically stable and maintain toxicity over time. Out of more than 350 mycotoxins identified in nature, aflatoxins, T-2 toxin, diacetoxyscirpenol, vomitoxin, zearalenone, ochratoxins, ergot alkaloids, oosporein, cyclopiazonic acid, and tricothecenes are the most common and important in poultry [5].

Mycotoxicosis and Their Effect in Poultry

Aflatoxicosis: The aflatoxins are toxic and carcinogenic metabolites such as Aspergillus flavus. Aflatoxicosis in poultry primarily affects the liver but can involve immunologic, digestive, and hematopoietic functions. Aflatoxin can adversely affect weight gain, feed intake, feed conversion ratio, pigmentation, carcass yield, egg production, male and female fertility, and large hatchability problems. Some effects are directly attributable to toxins, whereas others are indirect, such as reduced feed intake. Susceptibility to aflatoxins varies, but in general, ducklings, turkeys, and pheasants are susceptible, while chickens and Japanese quail are relatively resistant. Clinical signs vary from general unthriftiness to high morbidity and mortality. At necropsy the lesions are found mainly in the liver, which can be due to necrosis and congestion or yellow due to lipid accumulation. Hemorrhages may occur in liver and other tissues. In chronic aflatoxicosis, the liver becomes yellow to gray and atrophied.

Fusariotoxicosis: The genus Fusarium produces many mycotoxins injurious to poultry. The trichothecene mycotoxins produce caustic and radiomimetic patterns of disease exemplified by T-2 toxin and diacetoxyscirpenol (DAS). Deoxynivalenol (vomitoxin, DON) and zearalenone are common trichothecene mycotoxins that are relatively nontoxic for poultry but may cause disease in large concetratin in feed. Fusariotoxicosis in poultry caused by the trichothecenes results in feed refusal, caustic injury of the oral mucosa and areas of the skin in contact with the mold,acute digestive disease, and injury to the bone marrow and immune system [3]. Lesions include necrosis and ulceration of the oral mucosa, gastro intestinal mucosa, mottling of the liver, atrophy of the spleen and other lymphoid organs, and visceral hemorrhages. In laying hens, decreased egg production can be accompanied by depression, recumbency, feed refusal, and cyanosis evident in the comb and wattles [6]. Other Fusarium mycotoxins cause defective growth of long bones.

Ochratoxicosis: Ochratoxins are quite toxic to poultry. These nephrotoxins are produced chiefly by Penicillium viridicatum and Aspergillus ochraceus in grains and feed. Ochratoxicosis causes primarily renal disease but also affects the liver, immune system, and bone marrow. Severe intoxication causes reduced spontaneous activity, huddling, hypothermia, diarrhea, rapid weight loss, and death. Moderate intoxication impairs weight gain, feed conversion ratio, pigmentation, carcass yield, egg production, fertility, and hatchability [5, 6].

Ergotism: Toxic ergot alkaloids are produced by Claviceps spp, which are fungi that attack cereal grains. The mycotoxins form in the sclerotium, a visible, hard, dark mass of mycelium that displaces the grain tissue. Within the sclerotium are the ergot alkaloids, which affect the nervous system, causing convulsive and sensory neurologic disorders, the vascular system, causing vasoconstriction and gangrene of the extremities and the endocrine system, including neuroendocrine control of the anterior pituitary gland. In chicks, the toes become discolored due to vasoconstriction and ischemia. In older poultry, vasoconstriction affects the comb, wattles, face, and eyelids, which become atrophied and disfigured. Vesicles and ulcers develop on the shanks of the legs and on the tops and sides of the toes. In laying hens, feed consumption and egg production are reduced [6].

Mycotoxicosis Diagnosis in Poultry

Mycotoxicosis should be suspected when the history, signs, and lesions are suggestive of feed intoxication, and especially when moldy ingredients or feed are evident. Toxin exposure associated with consumption of a new batch of feed may result in subclinical or transient disease. Chronic or intermittent exposure can occur in regions where grain and feed ingredients are of poor quality or when feed storage is substandard or prolonged. Impaired production can be a clue to a mycotoxin problem, as can improvement because of correction of feed management deficiencies. Definitive diagnosis involves detection and quantitation of the specific toxins. This can be difficult because of the rapid and high volume use of feed and ingredients in poultry operations. Diagnostic laboratories differ in their respective capabilities to test for mycotoxins and should be contacted before sending samples. Feed and also poultry that are showing sings of sicknes or recently dead should be submitted for pathological examinatios. A necropsy and related diagnostic tests should accompany feed analysis if mycotoxicosis is suspected. Concurrent diseases can adversely affect production and should be considered. Sometimes, a mycotoxicosis is suspected but not confirmed by feed analysis. In these situations, a complete laboratory evaluation can exclude other significant diseases. Feed and ingredient samples should be properly collected and promptly submitted for analysis. Mycotoxin formation can be localized in a batch of feed or grain. Multiple samples taken from different sites increase the likelihood of confirming a mycotoxin formation zone. Samples should be collected at sites of ingredient storage, feed manufacture and transport, feed bins, and feeders [5, 6].

Prevention of Mycotoxicosis in Poultry

Prevention of mycotoxicoses should focus on using feed and ingredients free of mycotoxins and on management practices that prevent mold growth and mycotoxin formation during feed transport and storage. Regular inspection of feed storage and feeding systems can identify flow problems, which allow residual feed and enhance fungal activity and mycotoxin formation. Mycotoxins can form in decayed, crusted feed in feeders, feed mills, and storage bins, cleaning and correcting the problem can have immediate benefits. Temperature extremes cause moisture condensation and migration in bins and promote mycotoxin formation. Ventilation of poultry houses to avoid high relative humidity also decreases the moisture available for fungal growth and toxin formation in the feed. Antifungal agents added to feeds to prevent fungal growth have no effect on toxin already formed but may be cost effective in conjunction with other feed management practices [6]. Propionic acid are effective inhibitor, but the effectiveness may be reduced by the particle size of feed ingredients and the buffering effect of certain ingredients. Sorbent compounds such as hydrated sodium calcium aluminosilicate effectively bind and prevent absorption of aflatoxin. Esterified glucomannan, derived from the cell wall of the yeast Saccharomyces cerevisiae, is protective against aflatoxin B1 and ochratoxins. It reduces toxicity through the binding and reduction in bioavailability of fumonisins, zearalenone, and T-2 toxin. Various other fermentation products, algae and plant extracts, and microbial feed additives have demonstrated ability to bind or degrade mycotoxins and may be applicable and appropriate for the situation.

Acknowledgement

The paper is a part of the research work on the project III 46012 financed by the Ministry of Education, Science and Technological Development of the Republic of Serbia.

Read More Lupine Publishers Veterinary Sciences : https://lupine-publishers-dairy-veterinary.blogspot.com/

Read More Lupine Publishers Articles : https://lupinepublishers.blogspot.com/