Gizzard erosion and ulceration syndrome (GEU) in poultry are characterized by macroscopic defects in the koilin layer as well as defects and inflammation of the gizzard mucosa. The condition is seen in both layer and broiler chicken but the incidence is more in broilers. In literature, neither “erosion” nor ”ulceration” is clearly defined, but most researchers consider the defects affecting the koilin layer as ”erosions” whereas gross lesions affecting the mucosa have been designated as “ulcers”. GEU has been associated with many and diverse factors that have been assumed to play a causative, predisposing or preventive role. This syndrome is also called as Ventriculitis, Black vomit and Vomito negro.
GEU syndrome was reported for the first time in the 1930s. Early studies were mainly focused on nutritional deficiencies and peroxidation of highly polyunsaturated fatty acids as causative factors. Later the focus was moved towards toxic substances in the feed. In 1985, Scott reviewed the causes of this condition and concluded that gizzerosine in the feed causes overproduction of gastric acid leading to GEU. In the last decades, serotype 1 of fowl adenovirus A and Clostridium perfringens have been identified as major infectious causes for GEU in chickens. Although GEU is globally distributed and its subclinical form appears to be common in commercial poultry flocks, the condition did not get proper attention probably due to the lack of one definitive cause of the syndrome.
During the last decades, serotype 1 of fowl adenovirus A has been implicated as an important pathogenic agent in the development of GEU in chickens. Both vertical and horizontal transmission is important in the spread of adenoviruses. Broilers affected by adenoviral gizzard erosion usually show no clinical signs and the problem is therefore mainly detected at slaughter. Most virus strains that have been isolated from gizzard lesions belong to serotype 1 of fowl adenovirus A within the genus Aviadenovirus. Gizzard lesions associated with viral infections are characterized by small hemorrhagic foci to major bleeding, both on the proventriculus and gizzard.
The most important bacteria causing GEU are Clostridium species (Clostridium colinum, Clostridium perfringens, etc.) that grow in the anaerobic spaces of the transitional area. Clinical signs are dark necrosis affecting the transitional area and the upper part of the gizzard, with possible bleeding and increased mortality, usually appeared about 1 week after hatching, but outbreaks could appear in chickens up to 4 weeks of age. C. perfringens is capable of hydrolyzing the amide bond of conjugated bile salts and a protective effect of bile against GEU has been proposed. It is, therefore, possible that C. perfringens is more than an opportunistic pathogen occupying a new niche following the appearance of gizzard lesions. Prevention is carried out through improving the digestibility of feed and using bactericide plant extracts. For treatment, antibiotics might be necessary.
Feed contaminated with mold species like Aspergillus and Fusarium (more than 2 million spores/gram of feed), moldy bedding or moldy environment can cause lesions in the gizzard. The infection starts with a small brown protrusion in the cornea layer which leads to ulcers in a later stage. Cornea layer becomes very easy to detach and white fungal filaments can be observed under it. Acidifiers and anti-fungal compounds can help to ameliorate the lesions in this condition.
a) Deficiency of sulfur-containing amino acids (Methionine and Cysteine)
Gizzard erosions were prevalent and severe when chickens were fed inadequate methionine, which is an intermediate in the biosynthesis of taurine.
b) Deficiency of Selenium
c) Deficiency of vitamin E, B6 and B12
Vitamin E has been protective against GEU if substantial amounts of highly polyunsaturated fatty acids are present in the feed. Whole bile and bile components (including sodium taurocholate) have a protective effect against gizzard erosions. The role of vitamin B6 in taurine synthesis and B6 deficiency may contribute to taurine insufficiency and presumably also to insufficiency of taurocholic acid.
d) Grit and feed particle size
Access to grit and inclusion of at least 20% cereal particles larger than 1 mm in size in the diet will have a positive effect on the development and functioning of gizzard and it will also reduce the frequency and severity of GEU lesions in poultry.
e) Pelleted versus mash feed
The occurrence of GEU was lower in mash fed broilers with access to litter compared to pellet fed and without access to litter.
f) Non-soluble fibers
Ingestion of non-soluble fibers has been shown to exert strong effects on the structure and function of the gizzard. Inclusion of at least 3% coarse fibers in the feed increased the relative weight of the gizzard and reduced the pH of the gizzard contents suggesting a preventive effect of fiber on GEU.
Feed contaminated by Tricothecenes group (T-2 toxin, monoacetoxyscirpenol and diacetoxyscirpenol) of mycotoxins are capable of dissolving the cellular protoplasm of the cells located in the gizzard because of their caustic nature. These mycotoxins, after their absorption in the intestines pass to the blood and later to the saliva, causing lesions in the mouth and gizzard. Other mycotoxins like, moniliformin, fumonisins b1 and b2, deoxynivalenol, cyclopiazonic acid, oosporein and rubratoxin may have the potential to cause GEU. On the appearance of this condition, immediate withdrawal of contaminated feed and use of mycotoxin binders with high adsorption rates for trichothecenes helps to reduce the lesions.
b) Biogenic amines
Biogenic amines are by-products of the bacterial degradation of some amino acids, found mainly in ingredients of animal origin. The most commonly found biogenic amine is histamine, primarily produced in fish and fish products by time-dependent and temperature dependent bacterial processes. Free histidine is the precursor of histamine while other amino acids are precursors of other biogenic amines. Histamine stimulates the receptors located in the proventricular glands increasing the hydrochloric acid secretion and causing superficial gizzard erosion. Pure histamine is only able to induce gizzard erosions when present in high concentrations (>200 mg/kg) in poultry feed. The possibility of an interaction with gizzerosine, if present in the same feed, cannot be ruled out. Biogenic amines have also been reported from meat products as well as dairy products, so the potential source in the feed is not restricted to fish meal.
c) Gizzerosine in fish meal
Fish meal always has some potential of causing gizzard erosions in poultry. The lesions reported can include the presence of small cracks in the gizzard up to severe erosion and hemorrhage. When fish meal is overheated (130oc) during processing, the histidine or histamine present in the meal can react with lysine forming a chemical compound called gizzerosine. Gizzerosine is ten times as potent as histamine in enhancing acid production by the proventriculus. An obvious dose-dependent increase in gizzard erosions was noticed in chickens given concentrations from 0.15 mg gizzerosine/kg feed.
Various studies revealed the interaction between gizzerosine and mycotoxins. The toxic effects caused by gizzerosine will be increased, if the feed is contaminated with higher levels of aflatoxins. The modern processing of fish meal has to a large extent changed the drying process, lowering the maximum temperature well below the temperature said to be associated with the formation of high levels of gizzerosine. It is therefore likely that the levels of gizzerosine in general would be lower at present than previously. However, the old processing methods may still be in use in some parts of the world.
d) Copper toxicity (>250 ppm):
Due to its low price in many countries, up to 1 kg of copper sulfate (25% Cu) per ton is added to the feed as a growth promoter or as an antifungal agent. If the amount of copper in the feed is more than 250 ppm, it may cause erosions/ulcers in the gizzard. To prevent this problem farmers are advised to avoid overdosing of copper sulfate and to choose a reliable source that will not form clumps in the feed.
Restriction or deprivation of feed and/or water may increase the frequency and severity of gizzard erosion lesions whether this is initiated from the day of hatch or later in the rearing period of chicken.
Stress during incubation and/or hatching may cause gizzard erosions.
Gizzard lesions noticed in chick embryos and newly hatched broiler chicks indicate that GEU might be congenital and therefore caused and influenced by factors present before hatch. The incidence of GEU in newly hatched chicks may be linked to breeder diet, breeder age and capillary fragility combined by a transient rise in blood pressure levels during hatching.
Gizzard erosion and ulceration syndrome (GEU) is distributed worldwide and its subclinical form appears to be common in commercial poultry flocks. Over the past few years, serotype 1 of fowl adenovirus A and Clostridium perfringens infections, presence of gizzerosine and other biogenic amines have been identified as major causes for GEU in chickens. Lack of access to litter, use of animal-based feed ingredients like fish meal, meat bone meal, mycotoxin contamination and low fiber content in the feed are predisposing factors for GEU. Under practical situations, it is difficult to associate the gizzard lesions with only one etiologic agent, since they represent the result of the combination of several viral, nutritional and toxic agents like gizzerosine and mycotoxins. In this condition, an effective differential diagnosis by an experienced veterinarian is needed to determine what measures must be taken to control the problem.