In large-scale white-feather broiler production systems, gizzard and proventricular inflammation has evolved from a single digestive tract disease into a systemic syndrome affecting the entire production cycle. In clinical production, the intractable problem of “symptoms improving with medication, recurrence after medication is stopped, repeated treatment, and economic losses” is widespread.
Traditional diagnostic and treatment approaches in the industry have mostly focused on symptomatic medication, relying on drug treatment to address lesions. However, clinical practice has shown that the core reason gizzard and proventricular inflammation is difficult to cure is not a lack of preventive and control medications or insufficient efficacy. Rather, the chain of causation—centered on vertical transmission through breeding stock, incubation damage, feed toxin accumulation, and rearing stress—has already formed a complete cycle before chicks begin eating or receive their first medication.
A one-dimensional, symptom-focused diagnostic and treatment model cannot resolve a systemic disease problem caused by multiple overlapping factors. This is also the fundamental reason why current prevention and control efforts for gizzard and proventricular inflammation in broilers are ineffective.
I. A multidimensional pathogenic cycle: the core drivers of persistent gizzard and proventricular inflammation
The occurrence of proventriculitis and gizzard erosion in white-feathered broiler chickens is not caused by a single pathogen or a management error. Rather, risks across four dimensions—breeding stock, incubation, feed, and husbandry management—accumulate and reinforce one another, ultimately forming a cycle of irreversible pathological damage.
(I) Vertical transmission from breeding stock: congenital immune deficiencies and gastric damage during embryonic development
Risks in breeding stock are the primary underlying cause of early-onset and high-incidence proventriculitis and gizzard erosion. Reticuloendotheliosis virus and chicken infectious anemia virus can be transmitted vertically through hatching eggs, leaving chicks with congenital immunosuppression as soon as they hatch. Clinical necropsies show that 1-day-old chicks commonly have pathological changes such as mild proventricular edema and atrophy of the thymus and bursa of Fabricius.
Impaired development of immune organs directly causes a substantial increase in the threshold for immune responses in chicks. Their capacity for detoxification, anti-inflammation, and mucosal repair is congenitally inadequate. Consequently, all subsequent drug treatments and preventive interventions lack a normal physiological foundation in the host.
Meanwhile, mycotoxins in breeder diets can accumulate inside hatching eggs and continue to cause damage during embryonic development. By 18 days of incubation, characteristic black ulcerative lesions may appear on the keratin layer of the embryonic gizzard. Before chicks have started eating or drinking, organic damage to the digestive tract has already formed, laying an irreversible risk for an outbreak of glandular gizzard inflammation later on.
(b) Incubation stress: a key driver of initial digestive tract damage in chicks
Improper incubation management is a key factor that aggravates digestive tract damage in embryos and chicks and entrenches pathological defects, completing the “final step” in establishing gizzard damage in chicks. Excessive formaldehyde concentration when disinfecting hatching cabinets can directly burn the delicate digestive tract mucosa of chicks and damage the first immune barrier. Loss of control over temperature settings in the late incubation period can trigger abnormal, persistent gastric acid secretion in chicks. Without feed to neutralize it, the gastric acid continuously erodes the gizzard mucosa, causing starvation ulcers.
In addition, the practice commonly seen in large-scale farming of withholding feed and water from newly hatched chicks for more than 24 hours can further aggravate gastric acid self-digestion damage. All these types of mucosal damage occur in the early brooding period and are fully established before clinical drug prevention and control begins. Later drug intervention can only passively repair damaged tissue and cannot reverse the pathological basis at its root.
(Three) Feed mycotoxins: the core source of ongoing, hidden damage throughout the entire production cycle
Feed mycotoxin contamination is a persistent disease-causing factor throughout the entire broiler production cycle and a key driver of the rising incidence and severity of proventriculitis and gizzarditis in recent years. As a core energy ingredient in broiler feed, corn’s mold contamination directly determines the feed’s toxin load. Among these, T－2 toxin can directly corrode and ulcerate the proventricular and gizzard mucosal tissues, while vomitoxin can cause thinning of the proventricular wall, muscle relaxation, and digestive dysfunction.
Affected by extreme abnormal weather, the rate of corn mold contamination in the Huang-Huai-Hai main production areas has risen significantly. Some feed ingredients are blended with others to reduce costs, resulting in mycotoxin levels in finished feed exceeding safe thresholds and substantially increasing the risk of disease in flocks. Of particular note, mycotoxins can accumulate in the body and cause ongoing disease. After birds consume moldy feed, the toxins deposit in body tissues. Even if compliant feed is introduced later, accumulated toxins continue to damage the digestive tract and immune organs, fundamentally challenging the conventional belief that “changing the feed is enough for recovery.”
(Four) Environmental and management stress: the key triggers of disease outbreaks
Against a background of innate immune suppression, subclinical digestive tract damage, and toxin accumulation in the body, various environmental and husbandry stressors are key “trigger factors” for outbreaks and recurrent episodes of proventriculitis and gizzard inflammation. Climatic conditions such as high temperatures and humidity in summer and autumn, and day-night temperature differences exceeding 5℃ in autumn and winter, can disrupt neuroendocrine regulation and suppress the immune function and gastrointestinal digestion and metabolism of chickens.
Meanwhile, the combined pressures of excessive stocking density and stress from routine vaccination continue to deplete the flock’s immunity. The clinical pattern of concentrated onset of proventriculitis and gizzard inflammation after immunization at 7 days of age is precisely the concentrated clinical manifestation of subclinical pathological damage under stress.
In summary, various pathogenic factors form a chain of vicious cycles: vertical transmission causes immune suppression; immune suppression substantially reduces the body’s tolerance of mycotoxins and capacity for repair; the digestive tract mucosal barrier suffers ongoing damage, creating conditions for secondary infection by harmful bacteria; ultimately, this forms a persistent pathological loop of immune suppression—gastric mucosal damage—intestinal lesions—recurrent infection.
II. Root Cause of the Failure of Traditional Diagnosis and Treatment: Directional Cognitive Bias Matters More Than Differences in Medication
The biggest misconception in the prevention and control of broiler proventriculitis and gizzard inflammation is to simplistically define this systemic syndrome as a bacterial digestive tract disease or merely an abnormality in gastric acid secretion. This leads to a series of incorrect medication regimens that worsen bodily damage and make the disease recur more frequently.
Blindly administering high doses of antibiotics is effective only against a small number of secondary bacterial infections. It is completely ineffective against the core causes, such as vertical viral transmission, mycotoxin damage, and immunosuppression. At the same time, it severely disrupts the balance of beneficial intestinal bacteria and weakens the body's digestive and absorptive capacity and intestinal barrier function. The abuse of antipyretic and analgesic drugs directly aggravates gastrointestinal mucosal ulceration and bleeding, expanding tissue damage. Although conventional acid-suppressing drugs may temporarily relieve symptoms of gastric inflammation, administering them routinely to the entire flock suppresses normal gastric acid secretion in healthy chickens, causing a sharp decline in protein digestion and absorption rates and significantly impairing production performance.
Adsorbent mycotoxin-removal products such as montmorillonite have the drawback of non-selective adsorption: while adsorbing toxins in feed and the intestinal tract, they also adsorb large amounts of nutrients such as vitamins and trace elements. Long-term, indiscriminate use can lead to nutritional deficiencies and stunted growth in the flock, resulting in serious hidden production losses. If immunosuppression has not been reversed, accumulated toxins have not been cleared, and the pathological cycle has not been broken, all single-target symptomatic medications constitute ineffective intervention and cannot address the root cause of disease recurrence.
Three. Rebuilding a Precision Prevention and Control System: From Symptom Relief to Root-Cause Treatment
Given the characteristics of adenomyogastritis, which is often caused by multiple factors and develops through a closed-loop disease process, the traditional “symptomatic treatment” approach must be thoroughly abandoned. A tiered, orderly, and systematic prevention and control strategy should be established: first relieve inhibition and eliminate toxins, then repair the mucosa, and finally control secondary infections. This sequence must not be reversed, enabling a shift from passive treatment to proactive disease prevention.
(I) Early golden intervention: focus on blocking the root cause by addressing congenital defects in chicks
1～5 days of age is the golden window for preventing and controlling adenomyogastritis in white-feather broilers. At this time, immunosuppression caused by vertical transmission in chicks has not yet become fully established, and organic damage to the digestive tract is still at an early stage. The core of prevention and control at this stage is not symptomatic treatment of inflammation, but improving immune function, protecting the gastrointestinal mucosa, and reducing congenital damage to weaken the pathological basis at its source. Compared with firefighting-style treatment after disease develops, prevention and control at this stage costs less and is more effective.
(II) Precise diagnosis and treatment: manage flocks at different disease stages in tiers
For flocks already showing typical signs of proventriculitis and gizzard erosion, such as ruffled feathers, diarrhea with feed passage, reduced feed intake, and gastric mucosal ulcers, prioritize the use of classic compound traditional Chinese medicine preparations containing Astragalus, Atractylodes, Bletilla, and cuttlebone. These provide multiple benefits, including immune regulation, support for healthy qi and blood, and mucosal repair. Combine them with broad-spectrum, highly effective mycotoxin binders to comprehensively remove accumulated toxins from the body and break the pathological cycle.
Use antibacterial drugs precisely only after an antimicrobial susceptibility test confirms a clear secondary bacterial infection, and strictly control the dosage and course of treatment to prevent indiscriminate broad-spectrum antibacterial use and avoid secondary harm to the body caused by drug misuse. Firmly reject indiscriminate medication of the entire flock. Target treatment precisely at affected birds and high-risk subgroups. Do not use acid-suppressing drugs or mineral adsorbents as routine preventive medications for long-term supplementation.
Four. Final summary
The intractable nature of proventriculitis and gizzard erosion in white-feathered broilers essentially reflects a concentration of gaps across the entire chain, from breeder stock sanitation and hatching control to feed quality control and brooding management. Drug intervention can only serve as an auxiliary disease-control measure to relieve clinical signs, prevent worsening, and reduce farming losses; it cannot make up for management deficiencies across the entire production process.
In livestock production, only by moving beyond the entrenched mindset of relying on a single medication, recognizing the systemic, full-cycle, and cumulative characteristics of adenomyogastritis, closing prevention and control gaps across the entire process—from breeding stock, hatching, and feed to rearing, diagnosis, and treatment—and rebuilding a science-based prevention and control system of “prevention first, source tracing and control, precise treatment, and gradual repair” can the industry’s persistent challenge of recurrent adenomyogastritis be addressed at its root, stabilizing flock growth performance, reducing farming losses, and improving the economic benefits of large-scale farming.