Fusarium species are one of the major sources of mycotoxins affecting the gastrointestinal tract
A correct understanding of the causative agents of gastrointestinal lesions will help determine control measures.
Mycotoxins are always present in animal feed, albeit in varying amounts, and can affect various systems in poultry, such as the gastrointestinal tract (GIT) and internal organs.
They produce a variety of diseases, either directly or in combination with other major stressors such as pathogens, collectively known as "mycotoxicosis." Mycotoxin poisoning is characterized by symptoms including lesions that can be used to clinically diagnose the presence of mycotoxins. However, these injuries may not be solely caused by mycotoxins. They may be the result of different nutritional, management, and pathogenic conditions, so it is important to make a differential diagnosis, that is, to distinguish one disease or condition from others that exhibit similar symptoms, before drawing conclusions.
Mycotoxic lesions in poultry
GIT is the first system exposed to the effects of mycotoxins following ingestion. T-2 toxin (T-2), HT-2 toxin, deoxynivalenol (DON), monoacetoxy pinol (MAS) and diacetoxy pinol (DAS) from Fusarium-derived trichothecenes and cyclopizoic acid (CPA) from the Aspergillus flavus or Penicillium genus . are the major mycotoxins affecting the GIT.
These mycotoxins can cause oral lesions, crop necrosis, gizzard erosion, gastric adenitis, epithelial mucosal inflammation and intestinal bleeding.
T-2 toxin and DAS have a more corrosive effect than other toxins in this group and produce lesions in the oral cavity (tongue, beak, palate) and erosion in the gizzard. gizzard is also the primary organ affected by DON, which when high levels can increase gizzard weight and gizzard erosion.
Other mycotoxins that cause gizzard ulcers include candida and fumonisins B1 and B2. CPA affects the gastric gland mucosa and causes glandular gastritis. These mycotoxins dissolve the protoplasm of cells in the mucosa, and the saliva in the mouth promotes their adhesion to the mucosa. After being absorbed through the intestines, these mycotoxins are transferred to the circulatory system and returned to the mouth through saliva, again causing secondary damage in the mouth and possibly in the gizzard .
Differential Diagnosis
There are a variety of non-pathogenic or pathogenic conditions represented by GIT lesions. Most non-pathogenic causes are due to nutritional or management reasons, while pathological causes include living organisms such as fungi, protozoa, bacteria, and viruses.
Some situations that should be ruled out when considering mycotoxin poisoning are:
1. Nutritional status
Copper
Zinc
Choline chloride
Sulfur-containing amino acids
Vitamins (A, E, B6, biotin )
biogenic amines
fish meal
feed structure (feed/pellet)
feed ingredients (fiber content)
2. Management conditions
quaternary ammonium compounds (QAC)
hunger
hatching stress
beak removal
3. Pathogenic conditions
Thrush/ Candidiasis
Pseudomembranous colitis /Aspergillosis
Helminthiasis
Histomoniasis/Blackhead
Coccidiosis
Clostridium perfringens Infection
Clostridium perfringens caused by bacterial infection
avian pox virus
avian adenovirus
avian reovirus
pair Differential diagnosis of etiologic agents of GIT lesions is not easy, such as oral lesions, gizzard erosion, gastric adenitis, and intestinal necrosis . However, it is theoretically possible to differentiate microscopically between lesions caused by pathogenic agents and those caused by non-pathogenic causes.
Pathogenic pathogens capable of causing lesions in the GIT are characterized by a prominent lymphatic infiltrate, without which detection would be impossible.
Among the viral preparations listed, the localization of the infiltrate varies depending on the type of virus and the presence of typical viral lesions in other organs.
In the case of reovirus and adenovirus , the infiltrate is present in the muscular wall of the organ rather than in the glands, as it occurs in lesions arising from Marek's disease. Another important difference in lesions caused by Marek's disease is the presence of lymphoid infiltration in the neuroserosa layer of the outer wall of the gastric glands.
When GIT lesions are detected in the field, effective differential diagnosis will help determine what control measures should be taken. Under commercial poultry production conditions, it is difficult to link these lesions to just one pathogen, as they represent the result of a combination of multiple pathogens including mycotoxins, which are more likely to act together with the primary pathogen.
Several published experiments have shown that the association between mycotoxins and the drugs listed here (e.g., biogenic amines, gizzerosine, Aspergillus fumigatus , Clostridium spp.) can enhance negative effects (not only in terms of GIT lesions) . and reovirus, etc. Therefore, there is no doubt that mycotoxin-contaminated feed plays an important role in causing these lesions of GIT. Routine testing of feed samples for mycotoxins and understanding their effects would be a good start.
Mycotoxin risk management in poultry
Appropriate “mycotoxin risk management” tools are essential to protect poultry from mycotoxin hazards.
Mineral binders are often supplemented through feed to bind/adsorb various mycotoxins. However, trichothecenes (such as DON and T-2) have the lowest adsorption efficiency compared to polar mycotoxins (such as aflatoxin ). Since not all mycotoxins can be adsorbed by mineral binders, different strategies must be used to counteract mycotoxins with different properties.
Another key point to consider is that not all adhesives are the same and will exhibit different adsorption effects depending on their origin (e.g. inorganic or organic, composition, surface area, etc.).
For non-adsorbable mycotoxins, biotransformation is the main strategy to be followed, where microorganisms /enzymes change the structure of the mycotoxin into non-toxic metabolites.
Bioprotection is another strategy in which plant and algal extracts are used to provide hepatoprotection and overcome mycotoxin-induced immunosuppression, respectively. Therefore, a combination of strategies (adsorption + biotransformation + bioprotection) should be employed to counteract multiple mycotoxin challenges and mycotoxins.
Damage to the oral mucosa is caused by T-2 toxin
