Predisposing factors of gizzard erosion and control strategy in poultry

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INTRODUCTION

            In recent times, gizzard erosion and ulceration syndrome (GEU) have been very common in poultry at mild to moderate levels. The gizzard, also called a muscular stomach, is composed of a koilin (keratenoid) layer and an underlying mucosa35. Gizzard erosion and ulceration syndrome (GEU) are characterized by erosive lesions in the koilin layer of the gizzard and macroscopic defects in mucosa1. It was described and termed as ‘ventriculitis’2, ‘black vomit’3, ‘vomito negro’4, and ‘Muskelmagenerosionen5, in different published articles. The condition is seen in both layer and broiler chicken, but broilers have a higher incidence.

It usually causes reduced feed intake, growth, poor absorption of nutrients, and persistent diarrhea in birds, which leads to economic losses6. According to research, during GEU development, birds' feed intake and growth were significantly affected, and average body weight gain and feed consumption decreased by up to 12% and 14%, respectively. It affects various domestic birds with a prevalence of 1-50 % depending on species, region, and etiological factors7. In Bangladesh, the prevalence of GE (Gizzard Erosion) in broilers has reached 70.6-87.2%8. GEU has been associated with many diverse factors that have been assumed to play a causative, predisposing, or preventive role.

 

PREDISPOSING FACTORS OF GIZZARD EROSION

CONGENITAL FACTORS

            Gizzard and koilin lesions have been found in chick embryos and newly hatched broiler chicks, suggesting that GEU may be congenital and influenced by factors before hatch. GEU in newly hatched chicks may be linked to breeder diet, age, capillary fragility, and transient blood pressure increase during hatching9 (Figs. 1, 2, and 3).

 

STARVATION

            Newly hatched chicks deprived of feed and water experienced an increase in ulcerated gizzards, from 3 to 68% on day 4 post-hatch. Restriction or deprivation of feed and/or water may be associated with increased frequency and severity of lesions whether initiated on hatch day or later in the rearing period9.

 

NUTRITIONAL DEFICIENCIES

            Malnutrition status like deficiency of vitamin B6, vitamin B12, vitamin E, and decreased Sulphur-containing amino acids are associated with gizzard ulceration10. Vitamin B6 plays an important role in synthesizing taurine. Vitamin B6 deficiency results in taurine insufficiency, which results in insufficiency of taurocholic acid, and taurocholic acid means bile acid. Whole bile or bile components (including sodium taurocholate) have a protective effect against gizzard erosion11. Methionine is an intermediate in the biosynthesis of taurine. Inadequate methionine in the diet can cause prevalent and severe gizzard erosion12.

 

BIOGENIC AMINES AND GIZZEROSINE

            Feed microbial contamination will generate most biogenic amines (histamine) which catalyze the secretion of gastric acid13. Several bacteria can convert histidine into histamine, a biogenic amine linked to poor chicken performance. Histamine stimulates proventricular gland receptors, increasing hydrochloric acid secretion and causing superficial gizzard erosion14. Besides this, gizzerosine [2-amino-9-(4-imidazoyl)-7-azanonanoic acid] produced in poor-grade fish meals is an even more effective stimulator of gastric acid secretion in poultry15. Overheating fish meal during

processing the histidine or histamine present in the meal can react with lysine forming a chemical compound called gizzerosine16. Gastric ulcers are initiated and exacerbated by increased acid secretion and a weakened mucosal barrier.

COPPER SULFATE

            The adverse effect of high levels of copper sulfate in diets for poultry is gizzard erosion which means ulceration of the lining of the gizzard. It is most likely that the acidic nature of Cu (Copper) or sulfate dissociated from copper sulfate or even both may be responsible. Studies indicated that using extremely high amounts of copper additives (>300 ppm) results in liver cirrhosis, gizzard erosion, and kidney damage, which can seriously affect growth performance17.

 

RANCID FATS

            Rancid fats, particularly in hotter climates where fats readily become rancid if not stored properly; can cause feed passage issues in broilers, leading to lesions like proventriculitis, gizzard erosions, and enteritis18. This process involves the oxidation of fat and fat-soluble compounds, producing free radicals or reactive oxygen molecules.

 

TANNINS

            Tannins, polymeric phenolic compounds found in cereals, legumes, vegetables, and fruits, are a crucial secondary metabolite, consisting of nitrogen-free, hydrolyzed, and condensed forms. Tannins, which contain anti-nutritional content, negatively impact poultry, leading to performance losses such as reduced appetite, reduced feed intake, and poor nutrient absorption. They also cause bone disorders, pathological changes, irritation in the esophagus, necrosis in crops, gizzards, and duodenum, and can cause liver and kidney poisoning19.

 

ACETYLSALICYLIC ACID & SODIUM SALICYLATES

            Acetylsalicylic acid (ASA) and sodium salicylate (SS) are safe for poultry and commonly used in avian medicine due to their anti-inflammatory and analgesic properties. Studies have shown that a dose of 400 mg/kg of either ASA or SS can decrease weight gain and induce gizzard ulceration, which typically occurs in the transition zone between the glandular stomach and gizzard20.

 

MYCOTOXINS

            Trichothecenes are a group of Fusarium mycotoxins, including T-2 Toxin, Monoacetoxyscirpenol (MAS), Diacetoxyscirpenol (DAS), Deoxynivalenol (DON), and HT-2 toxins, which can cause gizzard erosion, oral lesions, and intestinal hemorrhage in the gastrointestinal tract. T-2 toxin and DAS are the most caustic, causing gizzard erosion. Cyclopiazonic acid (CPA) also causes mucosal necrosis in the gizzard21. Feed-borne mycotoxins like FB1, DON, AFB1, and OTA negatively impact intestinal epithelium integrity and cause necrotic enteritis and GEU in broiler chicks. Studies have reported impaired feed intake and growth in chickens during GEU development6.

 

VIRAL CAUSES

            Fowl adenovirus (FAV) is found in chickens, as evidenced by antibody surveys and high isolation rates in both healthy and sick birds. FAV is linked to a variety of diseases such as IBH, HPS, respiratory disease, necrotizing pancreatitis, and gizzard erosion22. Adenoviral inclusions in chicken gizzard epithelium show GEU lesions. Both vertical and horizontal transmission are crucial for adenovirus spread. Adenoviral gizzard erosion can be reproduced by horizontal transmission, and broilers affected usually show no clinical signs, mainly detected at slaughter. Gross lesions in the gizzard comprised mucosal injury that was ulcerative or necrotizing and koilin layer separation. According to histopathology, there was necrotizing ventriculitis with basophilic intranuclear inclusion bodies in the epithelial cells. Utilizing immunohistochemistry, egg culture, and electron microscopy, adenovirus-like particles were found22. Gizzard lesions often contain virus strains from serotype 1 of fowl adenovirus A, with FAdV-4 and FAdV-8 being the aetiologic agents in a few cases22.

 

BACTERIAL CAUSES

            Bacillus cereus (B. cereus) isolates have been found to causegizzard erosion and ulceration syndrome (GEU) in birds, potentially causing vomiting, diarrhea, or ulceration23. B. cereus can tolerate low pH by forming spores attached to the hydrophobic layer of gastric epithelium25. The koilin layer of the gizzard contains leucine proteins and arginine, which may help form biofilms, leading to stomach acid tolerance and metabolism23. Enterotoxins produced by B. cereus, Hbl, and Cytk genes, can cause dermonecrotic, cytotoxic, and hemolytic effects24. These toxins can reach their highest level during the late growth phase, causing damage to the koilin layer and mucosa of the gizzard, leading to long-term ulceration and diarrhea23.

            Clostridium perfringens was discovered to be an opportunistic bacterium in commercial chickens with gizzard ulcerations, and the severity of the lesions was observed to considerably increase caecal numbers26.

DIFFERENTIAL DIAGNOSIS

            Establishing a differential diagnosis between agents causing gizzard erosion and ulcerative syndrome in poultry is challenging. Gizzard erosion can be caused by multiple factors simultaneously. To address this, focus on non-infectious factors such as breeder management, Adenoviral vaccination, feed formulation, anti-nutritional factor(tannin), hatchery management, litter management, starvation history, and commercial poultry feed formulation (especially, vitamin-mineral premix, amino acids, quality and quantity of fish meal and amount of copper sulphate). Deviation from any of these factors can lead to gizzard erosion.

            Adenoviruses can cause GE, causing macroscopic damage in other organs. The liver is pale, friable, and enlarged, with focal or diffuse necrosis. Degenerative and necrotic changes in the liver cause dysfunction and decrease blood osmotic pressure, leading to straw-colored fluid accumulation in the pericardial sac27. Basophilic intranuclear inclusion bodies are present in hepatocytes, surrounded by a clear halo or filling the entire nucleus which are absent from other casual agents28.

            Mycotoxins causing gizzard erosion (GE) typically cause macroscopic damage in other organs, including bursal atrophy, enteritis, diarrhea, and mouth lesions. Under field conditions, mycotoxins affect multiple organs, and typical changes in organs like the thymus should be present when T2 toxin or DAS cause gizzard damage. Mycotoxin levels in feed can be identified by High-Performance Liquid Chromatograph (HPLC) which are rapid analysis, and detection at low levels with improved accuracy, good repeatability, and reproducibility29.

 

CONTROL STRATEGY

  • The inclusion of grit and at least 20% larger cereal particles larger than 1 mm in size in poultry diets can positively impact the development and functioning of gizzards and reduce the frequency and severity of GEU lesions30.
  • The study found that non-soluble fibers significantly impact the structure and function of gizzards, with at least 3% coarse fibers in feed increasing gizzard weight and reducing pH, suggesting fibers may prevent GEU damage30. To improve gizzard condition to eliminate rancid fat and tannins like antinutritional factors from diet.
  • Proper monitoring is required to avoid starvation in the early stages of chicks. Good brooding management, a proper number of feeders and drinkers, and a balanced diet can improve the feed intake of chicks. Another thing to be aware of is that farmers should avoid using sawdust as litter material because chicks can mistake sawdust for feed, and in the process, they consume it in good quantity, which leads to gastrointestinal impaction, mechanical injury in the gizzard and ultimately results in death.
  • Broiler feed formulation should prioritize vitamin E, B6, B12, and sulfur-containing amino acids to prevent nutritional deficiencies. Vitamin E is protective against GEU if there are high polyunsaturated fatty acids in feed10. Vitamin B6 and methionine are crucial in broiler nutrition as they aid in taurocholic acid or bile acid synthesis, preventing gizzard erosion31.
  • To reduce the effects of biogenic amine or gizzerosine, low-quality fish meal should be avoided. In the modern processing of fishmeal, the drying process has changed large extent, using low temperatures to reduce gizzerosine levels.
  • Judicious use of salicylates as drinking water medications and avoid overdoses. Copper sulfate is used very carefully as a water sanitizer and antifungal in feed and feed ingredients. An important factor to take into consideration to prevent this problem is to avoid overdosing and to choose a reliable source that will not form clumps in the feed.
  • Feed-borne mycotoxins can cause necrotic enteritis and GEU in broiler chicks, affecting intestinal epithelium integrity7. Using broad-spectrum mycotoxin binder can reduce mycotoxin-related risks in animal nutrition and production, as minimal/negligible binding of Vitamin B6 and Vitamin E and non-digestible mycotoxin binders facilitate excretion through excreta without gastrointestinal tract absorption.
  • The spread of avian adenovirus among flocks can be reduced through awareness and proper biosecurity measures. Separating infected and non-infected breeding flocks and vaccination of affected birds can be done. Inclusion body hepatitis vaccination to parent stock has been shown to pass protective titers to progeny and should be considered. Commercial vaccines are commonly used for serotypes 4 and 8, and broilers are vaccinated at <10 days of age when their parents lack serotype-specific antibodies32.
  • The antimicrobial factor produced by Bacillus subtilis PB6 is broadly active against various strains of Clostridium species33.

 

CONCLUSION

            Gizzard erosion and ulceration syndrome (GEU) is a global issue affecting commercial poultry flocks, affecting digestion and immune responses. This poses a threat to food safety and public health. GEU is caused by a combination of viral, nutritional, and toxic agents, making it difficult to identify a single etiologic agent. To prevent and control GEU, long-term monitoring and surveillance are necessary, along with effective differential diagnosis by experienced veterinarians.

 

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