Mycotoxins produce a variety of diseases, collectively known as “mycotoxicosis”, directly or in combination with other primary stressors such as pathogens. These diseases are exhibited by symptoms and lesions, which can be used to clinically diagnose the presence of mycotoxins.
However, these lesions are not just specific to mycotoxins and are also caused by diverse nutritional, management and pathogenic conditions. Hence it is significant to differentially diagnose these symptoms—i.e. to distinguish a disease or condition from others presenting with similar signs—before arriving at a conclusion. This article reviews the differential diagnosis of various conditions that cause similar lesions as mycotoxins in the GIT of chickens.
The GIT is the first system exposed to the effects of mycotoxins upon ingestion. T-2 toxin (T-2), HT-2 toxin, deoxynivalenol (DON), monoacetoxyscirpenol (MAS) and diacetoxyscirpenol (DAS) from the Fusarium-derived trichothecenes group, and cyclopiazonic acid (CPA) from either Aspergillus flavus or Penicillium fungi, are the primary mycotoxins that affect the GIT. These mycotoxins are capable of causing oral lesions, crop necrosis, gizzard erosion, proventriculitis, inflammation of epithelial mucosa and intestinal hemorrhage.
T-2 and DAS have a more caustic effect compared to other toxins in the group, and produce lesions in the mouth (tongue, beak, palate) as well as erosion in the gizzard. The gizzard is the primary organ affected by DON. At high concentrations, DON affects the gizzard by increasing gizzard weight and causing gizzard erosion. Other mycotoxins that affect the gizzard and cause gizzard ulcers include moniliformin and fumonisin B1 and B2.
CPA affects the mucosa of the proventriculus and causes proventriculitis. These mycotoxins dissolve the protoplasm of cells in the mucosa, and the presence of saliva in mouth for instance, facilitates their adherence to the mucosa. Upon their absorption through intestines, they are translocated into the circulation and reach back to the oral cavity through saliva, again causing secondary lesions in the mouth and possibly in the gizzard.
What causes lesions?
There are a variety of conditions, of either non-pathogenic or pathogenic origin, that cause lesions in the GIT. The majority conditions of non-pathogenic etiology are contributed by either nutritional causes or management procedures, while the pathologic etiologic agents include living organisms such as fungi, protozoa, bacteria and virus. Some of the frequent conditions that should be ruled out when considering mycotoxicoses are listed in Table 1.
Table 1. Conditions that may be related to lesions in the GIT.
When GIT lesions are detected in the field, an effective differential diagnosis will help determine the measures to be taken to control the condition. Under commercial conditions, it is difficult to associate these lesions with only one etiologic agent, since they represent the result of the combination of several agents including mycotoxins, which are more prone to act along with a major causative agent.
Several published experiments have demonstrated potentiation of the negative effects (not only in terms of lesions in GIT) caused by the association between mycotoxins and the agents listed here, such as biogenic amines, gizzerosine, Aspergillus fumigatus, Clostridium spp., and reovirus, etc. Hence, there is no doubt that feed contamination with mycotoxins play an important role in causing these lesions in the GIT.
The routine testing of feed samples for mycotoxins, as well as an understanding of the effects of mycotoxicosis, will be a good start towards preventing such lesions.