The stakes are considerable. Campylobacter is a leading bacterial cause of food-borne illness worldwide, and poultry meat is the dominant route of human exposure, whether through undercooked products or cross-contamination in the kitchen. In commercial broiler flocks, colonisation rates commonly range from about 55 percent to 100 percent, meaning the chicken intestinal tract functions as a vast reservoir of the pathogen. At slaughter, leakage of caecal contents can contaminate carcass surfaces, amplifying risk along the entire food chain. Because the caecal load of Campylobacter at the end of rearing is the strongest single predictor of carcass contamination, interventions that act inside the living bird have long been a priority for food-safety researchers.

The new analysis, conducted by Muhammet Kuddusi Erhan of Ağrı İbrahim Çeçen University in Türkiye, searched PubMed, Scopus and Google Scholar for controlled in vivo broiler trials published between January 2000 and July 2025. Following PRISMA 2020 guidelines, the review identified twelve eligible studies, eleven of which contributed fifteen separate comparisons to the quantitative syntheses. The author used random-effects models, taking the mean difference in log10 colony-forming units per gram of caecal contents as the effect measure for colonisation, and the standardised mean difference for growth performance, with pre-planned subgroup, dose-response and sensitivity analyses layered on top.

The headline result is striking. Across all routes of administration, caprylic acid supplementation reduced caecal C. jejuni loads by a pooled 1.46 log10 CFU per gram, a statistically significant reduction with a 95 percent confidence interval running from 2.50 to 0.41. But the pooled figure concealed enormous heterogeneity between studies, with an I-squared value of 88.1 percent, indicating that the trials were estimating genuinely different underlying effects rather than a single common one. Locating the source of that inconsistency turned out to be the most scientifically valuable part of the entire exercise.

When the comparisons were stratified by route of administration, the picture snapped into focus. In-feed application reduced colonisation by a pooled 2.68 log10 CFU per gram, with only moderate residual heterogeneity, whereas delivery via drinking water produced essentially no detectable effect at all. The formal test for subgroup differences was unambiguous, and the fall in heterogeneity from 88.1 percent overall to 39.0 percent within the in-feed subgroup identified the delivery matrix as the principal determinant of efficacy. Within the in-feed trials, 0.7 percent caprylic acid given for three to ten days cut caecal counts by 2.0 to 3.9 log10 units in three independent experiments, spanning both prophylactic use in young chicks and therapeutic use in market-aged birds.

The mechanism behind this route dependence is biologically plausible. Caprylic acid is bactericidal against C. jejuni in vitro at low millimolar concentrations, inserting into and disrupting bacterial membranes, interfering with the electron transport chain, lowering intracellular pH and inhibiting key metabolic enzymes. Feed, however, provides a lipophilic, slow-release matrix in which the undissociated fatty acid can survive passage through the upper gastrointestinal tract. Aqueous formulations, by contrast, appear to be rapidly absorbed by enterocytes before ever reaching the caeca, where C. jejuni colonises the mucus layer and is shielded from fatty acid activity. Consistent with this interpretation, raising the water-borne concentration thirty-two-fold produced no graded response whatsoever, suggesting the limiting step is survival en route rather than the quantity administered.

Equally important is what the analysis found about growth. Across nine comparisons, caprylic acid had no overall effect on growth performance, with a pooled standardised mean difference of +0.16 that was statistically indistinguishable from zero. This growth neutrality is what makes the compound economically viable as a pathogen-reduction tool. But the dose-response analysis revealed a clear ceiling. In-feed concentrations between roughly 0.35 percent and 0.875 percent produced consistent reductions of 2.2 to 3.6 log10 units, while higher concentrations became both weaker on average and markedly less reproducible. At 1.4 percent of feed, body weight was significantly depressed, with feed consumption falling steadily across the dose series. Palatability, it seems, imposes an upper practical limit before any pharmacological ceiling is reached, although reduced intake alone does not fully explain the loss of antimicrobial efficacy, since total caprylic acid consumption still rose with dose.

The author is candid about the limitations of the evidence base. Funnel-plot asymmetry was statistically significant, which in principle signals publication bias, but in this dataset the asymmetry maps precisely onto the feed-versus-water contrast: the imprecise, strongly negative comparisons are the in-feed trials, and the precise, near-null comparisons are the drinking-water trials. Genuine subgroup heterogeneity can generate funnel asymmetry as readily as selective publication, and with only six colonisation comparisons no statistical procedure can adjudicate between the two explanations. The pooled estimate of 1.46 log10 units should therefore be read as an upper bound on the true average in-feed effect. A leave-one-out analysis showed the direction of the effect was robust to the removal of any single comparison, though its statistical significance depended marginally on the largest trial. The apparently positive growth responses to caprylic acid blends also warrant caution, since in those comparisons the compound’s contribution could not be separated from that of other bioactive ingredients.

Why does the magnitude matter so much? Quantitative risk assessment indicates that a two-log reduction in carcass contamination would reduce the incidence of human campylobacteriosis associated with chicken meals roughly thirty-fold. The in-feed effect documented here, averaging 2.68 log10 units, comfortably exceeds that threshold, which is why the author argues that caprylic acid deserves a place within integrated Campylobacter control strategies for producers seeking antibiotic-free alternatives. The analysis also suggests that micro-encapsulated or otherwise protected formulations, which prolong the presence of fatty acids in the lower gut, deserve direct examination, and that future work should explore combinations with competitive exclusion cultures, bacteriophages or vaccination.

The broader significance of the study lies in its framing. Rather than treating antimicrobial efficacy and growth performance as unrelated endpoints, the review evaluates caprylic acid explicitly as a product-quality intervention, in which microbiological safety and zootechnical performance are assessed jointly. An additive that lowers pathogen load at the cost of impaired growth, or that improves growth without any food-safety benefit, has limited practical value. By converging on the same recommendation from both directions, an effective in-feed range of approximately 0.35 to 0.875 percent that delivers the antimicrobial benefit without a measurable productivity cost, the analysis offers the poultry industry something it has rarely had on this question: a quantitatively grounded, honestly caveated prescription. As antibiotic growth promoters remain banned in the European Union and increasingly restricted elsewhere, evidence of this kind may prove essential to making antibiotic-free poultry production both safer and commercially sustainable.

Subject of Research: Effects of dietary caprylic acid on Campylobacter jejuni colonisation and growth performance in broiler chickens

Article Title: Dietary caprylic acid, Campylobacter jejuni colonisation and product quality in broilers: a systematic review and meta-analysis

Article References: Dietary caprylic acid, Campylobacter jejuni colonisation and product quality in broilers: a systematic review and meta-analysis. (n.d.). https://doi.org/10.5194/aab-69-477-2026

Image Credits: AI Generated

DOI: 10.5194/aab-69-477-2026

Keywords: caprylic acid, Campylobacter jejuni, broiler chickens, food safety, meta-analysis, feed additives, medium-chain fatty acids, poultry production, antibiotic-free, dose-response, gut microbiology, zoonoses

A new study published in Veterinary Medicine and Science suggests that a carefully chosen pair of feed enzymes can dismantle many of those barriers. Researchers set out to determine whether phytase, protease, or the two together could alleviate the digestive limitations imposed by canola seed in broiler chickens, with a practical eye on which single enzyme delivers the most value when budgets allow only one. The question matters commercially: with protein-rich feed ingredients fluctuating wildly in price, industry stakeholders want to know exactly where their enzyme dollars are best spent.

The experiment involved 300 one-day-old male Ross 308 chicks, distributed in a completely randomised design across five treatments with five replicates of twelve birds each. One group received a corn-soybean meal control diet with no canola seed. A second received a diet containing 10 percent canola seed without enzymes. The remaining three groups ate the canola-seed diet supplemented with protease, with phytase, or with both enzymes together. Protease was included at 0.15 grams per kilogram of feed and phytase at 0.05 grams per kilogram. Birds were raised through starter, grower and finisher phases spanning 42 days, with feed and water available freely and standard vaccination protocols against Newcastle disease and infectious bursal disease applied.

The canola seed itself was thoroughly characterised before the trial began. Analysis showed 21.25 percent crude protein, a striking 42.76 percent ether extract, 18.39 percent crude fibre, and a gross energy content of 7063 kilocalories per kilogram. The seed also contained 5264 milligrams per kilogram of phytate phosphorus, 0.36 percent tannins and 9.37 micromoles per gram of glucosinolates, the very compounds suspected of constraining bird performance. Diets were formulated to be nutritionally comparable across treatments, with the canola diets naturally higher in fat and linoleic acid owing to the oil-rich seed.

The performance results told a clear story. Birds fed the unsupplemented canola diet ate significantly less, gaining roughly 6 to 7 grams less feed per day during the starter phase than controls, and their body weight gain suffered accordingly across the starter, grower and overall periods. Feed conversion ratio was also worse in the canola group during the grower phase. But adding enzymes changed the picture. Protease alone improved weight gain and feed intake relative to the canola-only diet, though its effect on intake was modest. Phytase alone produced a more pronounced lift in feed intake. The combination of both enzymes, however, was the standout: birds on the dual-enzyme diet ate and grew at rates statistically indistinguishable from the soybean-fed controls, effectively erasing the canola penalty.

Digestibility data revealed why. Apparent metabolisable energy, which fell to around 2687 kilocalories per kilogram in the canola-only group, rebounded to control levels of roughly 2860 kilocalories per kilogram in the phytase and combination groups. Crude protein digestibility told an equally interesting tale: the protease and combination diets actually exceeded the control diet, reaching about 74 to 75 percent digestibility compared with 71.7 percent in the soybean control. Ash and crude fibre digestibility were also restored by phytase-containing treatments. In other words, the enzymes did not merely compensate for canola’s drawbacks; in the case of protein digestion, they pushed nutrient utilisation beyond what the conventional soybean diet achieved.

The physiological mechanisms behind these gains emerged from a battery of measurements on the birds’ digestive systems. At 10 days of age, when the endogenous enzyme system is still immature, activities of amylase, lipase and total protease in the jejunum were depressed in the canola-only group but elevated in all enzyme-supplemented groups, with the combination treatment producing the highest amylase and lipase values. By day 42, when the birds’ own digestive machinery had matured, these differences had disappeared, underscoring that exogenous enzymes matter most in early life. Jejunal morphology followed a similar pattern: villus height and the villus-height-to-crypt-depth ratio, key indicators of absorptive capacity, were significantly higher in phytase and combination groups, while the canola-only diet drove deeper crypts, a sign of increased epithelial turnover under intestinal stress.

The gut microbiota and the physical properties of the intestinal contents added further layers of explanation. At day 10, birds on the combination diet harboured the highest Lactobacillus populations and the lowest Escherichia coli counts in the ileum, while Clostridium perfringens was lowest in that group compared with the canola-only treatment. Intestinal digesta viscosity, a critical determinant of how easily nutrients diffuse to digestive enzymes, was significantly elevated in the duodenum and jejunum of canola-fed birds but reduced by enzyme supplementation, particularly in the ileum. The researchers attribute this to phytase disrupting viscous phytate-protein complexes and protease breaking down peptide-fibre networks, together creating a more fluid digestive environment where enzymes and substrates can interact efficiently.

Perhaps the most striking findings concerned bone health. The unsupplemented canola diet significantly impaired tibia development: bones were lighter and shorter, breaking strength dropped to about 3074 newtons compared with 4279 newtons in controls, and bone ash, calcium and phosphorus percentages all declined. These deficits trace directly back to phytate, which forms insoluble complexes with essential minerals and renders them unavailable for skeletal mineralisation. The protease-plus-phytase combination restored bone weight, length, strength and mineral chemistry to levels comparable with or exceeding the control group, with bone ash reaching 41.93 percent and calcium 15.57 percent. The authors note that improved protein digestibility from protease likely supported collagen matrix synthesis, providing the organic scaffold upon which calcium and phosphorus are deposited, while phytase liberated the minerals themselves.

The study’s conclusion carries real weight for feed formulators. Replacing soybean meal with 10 percent canola seed without enzyme support demonstrably harms growth, gut function and bone mineralisation in broilers. Yet the combined application of protease and phytase overcame these constraints, performing better than either enzyme alone. The synergy is mechanistically elegant: phytase dismantles the structural and chemical barriers that phytate erects around proteins and minerals, creating conditions in which protease can work more effectively, while protease maximises the value of the nutrients phytase releases. For producers weighing enzyme purchases against volatile protein prices, the message is that the two enzymes are genuinely complementary, and that canola seed, long treated as a second-tier ingredient, can approach soybean meal performance when the right enzymatic tools are applied.

Subject of Research: Effects of protease and phytase supplementation on growth performance, nutrient digestibility, gut health and bone mineralisation in broiler chickens fed canola seed diets

Article Title: Protease and Phytase Alleviate Digestive Limitations of Canola Seed in Broiler Chickens

Article References: Sheikh‐Nazari, R., Jafari‐Khorshidi, K., & Jafari, M. A. (2026). Protease and Phytase Alleviate Digestive Limitations of Canola Seed in Broiler Chickens. Veterinary Medicine and Science, 12(6), Article e71259. https://doi.org/10.1002/vms3.71259

Image Credits: AI Generated

DOI: 10.1002/vms3.71259

Keywords: broiler chickens, canola seed, phytase, protease, soybean meal replacement, nutrient digestibility, gut microbiota, intestinal morphology, tibia mineralisation, antinutritional factors, feed enzymes, poultry nutrition

The experiment began with fifty one-day-old yellow-feather broilers, housed in standard cages under a controlled 16-hour light and 8-hour dark cycle and fed a commercial diet. At 28 days of age, the birds were sorted into body-weight-matched pairs and randomly assigned to two groups. One group received daily subcutaneous injections of corticosterone—the principal stress hormone in birds—at a dose of 4 milligrams per kilogram of body weight for seven consecutive days. The control group received injections of a 15% ethanol solution at the same volume. This corticosterone regimen is a well-established way to simulate chronic stress in poultry, allowing researchers to isolate the hormonal component of stress without confounding factors such as heat, crowding, or transport.

The physiological consequences were swift and clear. After 35 days, corticosterone-treated broilers had significantly lower final body weights and reduced average daily gain compared with controls. Paradoxically, they ate more: average daily feed intake rose significantly, and the feed-to-weight ratio worsened, meaning the stressed birds converted feed into body mass far less efficiently. The authors suggest this pattern reflects a metabolic shift under chronic stress, with energy diverted toward fat deposition through increased proteolysis and gluconeogenesis—essentially, the birds were burning muscle to fuel a stress response while consuming more feed overall.

Behavioral testing, conducted on days 35 and 36 using video-recorded encounters between unfamiliar birds from the same treatment group, revealed a striking escalation in aggression. Corticosterone-exposed chickens pecked their opponents significantly more often, and the total number of aggressive acts rose sharply. The effect spanned the social hierarchy: both dominant birds—identified by how frequently their opponents avoided them—and subdominant birds showed elevated aggression, though dominant individuals displayed the strongest increases, including more twisting attacks. This aligns with earlier observations that dominant animals may have aggression reinforced through mesolimbic reward circuitry, and with prior reports that prenatal corticosterone exposure and social stress both heighten injurious pecking in hens.

Crucially, the team also measured serotonin, the neurotransmitter long associated with behavioral inhibition. Chronic corticosterone significantly reduced serotonin concentrations in the hypothalamus—a key brain region for stress regulation—while paradoxically increasing serotonin levels in the plasma. Dopamine levels in the plasma, hippocampus, and hypothalamus remained unchanged. Because more than 90% of the body’s serotonin is produced by enterochromaffin cells in the gut, and because peripheral serotonin cannot cross the blood-brain barrier, this split pattern points to a gut-centered mechanism: stress may boost peripheral serotonin synthesis while starving the brain of the tryptophan precursor it needs to maintain central serotonergic tone. Low central serotonin activity is consistently associated with heightened aggression and impulsivity across species, from fish and rodents to humans.

Sequencing of the cecal microbiota added a microbial dimension to the story. Overall diversity metrics told a subtle tale: seven alpha-diversity indices showed no significant differences between stressed and control birds, and principal coordinate analysis based on Bray-Curtis distances found their community structures broadly similar. Firmicutes and Actinobacteria dominated both groups, with Faecalibacterium, Bifidobacterium, and Lactobacillus as the most abundant genera. But linear discriminant analysis effect size screening identified 29 differentially abundant taxa. Stressed birds carried more Shigella, Holdemania, and Clostridium, and fewer Desulfovibrio, Cellulosimicrobium, Enterococcus, Coriobacteriaceae, and Bacteroidales.S24_7. The message is that chronic stress reshapes the gut ecosystem in targeted ways rather than broadly collapsing it.

The metabolomics analysis, performed on plasma using ultra-high-performance liquid chromatography coupled to an Orbitrap mass spectrometer, identified 281 metabolites, of which 53 differed significantly between groups—23 upregulated and 30 downregulated under stress. Pathway enrichment pointed to tryptophan metabolism, pantothenate and CoA biosynthesis, and beta-alanine metabolism as the most affected networks. Tryptophan and its derivatives were upregulated in the plasma of stressed birds, even as hypothalamic serotonin fell. The researchers propose that immune activation under chronic stress may divert tryptophan away from serotonin production and into the kynurenine pathway, whose rate-limiting enzymes, IDO and TDO, are highly responsive to inflammatory cytokines. Kynurenine pathway metabolites such as quinolinic acid are themselves neuroactive and have been implicated in behavioral disorders.

Spearman correlation analyses then wove the threads together. Aggressive behavior correlated positively with the genus Clostridium and negatively with Actinomycetales and Coriobacteriaceae—relationships the authors note had not been described before. Clostridium, in turn, correlated positively with indole, L-tryptophan, and butyryl-L-carnitine, while Actinomycetales and Coriobacteriaceae tracked with beneficial compounds such as niacinamide and salicylic acid. Of 31 metabolites linked to the three key microbial taxa, 18 were also associated with aggression, including indole, L-tryptophan, biochanin A, niacinamide, leucodopachrome, and pyroglutamic acid. The mechanism may run through the vagus nerve: Clostridium species are known to metabolize tryptophan into neuroactive indoles and tryptamines that stimulate vagal afferents, and microbial metabolites such as kynurenine and indole derivatives are ligands for the aryl hydrocarbon receptor, a regulator of intestinal immune tone that can further bias tryptophan toward the kynurenine route.

The findings carry immediate practical weight for an industry where aggression translates directly into economic loss—non-beak-trimmed hens, for instance, show roughly a tenfold increase in mortality from aggressive pecking. The authors outline nutrition-based interventions supported by prior work: ensuring adequate dietary tryptophan, with commercial target tryptophan-to-lysine ratios around 16 to 19 percent, can support serotonergic tone and reduce abnormal pecking; probiotics such as Lactobacillus rhamnosus and Bacillus subtilis have been shown to mitigate stress-linked injurious behavior; and sodium butyrate, a microbial postbiotic, counters corticosterone-induced oxidative stress. The team is careful to stress that correlation is not causation, and that the observed taxa-metabolite-behavior links should be validated under different housing systems, stocking densities, lighting programs, and diets. Future experiments using fecal microbiota transplantation from donors with divergent stress phenotypes, gnotobiotic colonization, and targeted tryptophan manipulation could establish whether these gut communities truly transfer aggressive tendencies—a question made more plausible by mammalian studies in which microbiota transfer has conveyed anxiety- and depression-like behaviors between animals.

Subject of Research: Gut microbiota and plasma metabolite mechanisms underlying stress-induced aggressive behavior in broiler chickens

Article Title: Integrative analysis of gut microbiota and plasma metabolites reveals mechanisms underlying aggressive behavior in chronically stressed broiler chickens

Article References: Wu, X., Zhang, J., Ren, H., Cheng, X., Gao, J., & Ma, W. (2026). Integrative analysis of gut microbiota and plasma metabolites reveals mechanisms underlying aggressive behavior in chronically stressed broiler chickens. Stress Biology, 6(1), Article 30. https://doi.org/10.1007/s44154-026-00297-2

Image Credits: AI Generated

DOI: 10.1007/s44154-026-00297-2

Keywords: gut microbiota, broiler chickens, chronic stress, aggressive behavior, tryptophan metabolism, serotonin, corticosterone, metabolomics, microbiota-gut-brain axis, Clostridium, animal welfare, poultry science

The trial involved 300 one-day-old male Cobb 500 broiler chicks, randomly assigned to five dietary treatments with four replicate pens of 15 birds each. One group received a standard corn–soybean meal control diet, while the others were fed diets supplemented with either 0.75 percent or 1.5 percent Prangos ferulacea powder, or with 750 or 1500 milligrams per kilogram of the plant’s aqueous extract. All diets were formulated to be isocaloric and isonitrogenous, meaning they delivered equivalent levels of energy and protein, so any differences between groups could be attributed to the plant material itself rather than to nutritional imbalances. The birds were monitored over a full 43-day production cycle spanning starter, grower, and finisher phases.

The plant material itself carried considerable biochemical promise. Prangos ferulacea is native to West Asia and is rich in monoterpenes, coumarins, and phenolic compounds — classes of molecules frequently associated with antioxidant, antimicrobial, and smooth-muscle-modulating activity. The researchers harvested mature aerial parts of the plant from the rangelands of Divandareh County in Kurdistan Province, shade-dried them, and milled them into powder. To prepare the aqueous extract, ten kilograms of powder were macerated in thirty liters of distilled water for twenty-four hours, filtered, and concentrated at sixty to seventy degrees Celsius, yielding roughly 10.8 percent of the starting weight as dried extract. Botanical identity was confirmed by a qualified botanist, and a voucher specimen was deposited in the university herbarium, lending the study a level of taxonomic rigor that is not always present in phytogenic feed research.

When it came to the bottom line of broiler production — body weight gain and feed conversion ratio — the results were sobering. Across the entire 43-day period, cumulative body weight gain and feed efficiency did not differ significantly among the five dietary groups. Body weights at eleven, twenty-three, and forty-three days of age were statistically indistinguishable. There was, however, a phase-specific wrinkle: during the finisher period from days twenty-four to forty-three, body weight gain was significantly reduced in the supplemented groups compared with the control, a pattern the authors suggest could relate to effects on feed intake or palatability, though the underlying cause was not directly measured. Feed intake during the grower phase was actually higher in all supplemented groups, yet this did not translate into better growth, and overall feed intake across the trial was unaffected.

Carcass characteristics told a similarly restrained story. Carcass yield and the relative weights of the heart, liver, spleen, pancreas, and bursa of Fabricius were comparable across treatments. One exception stood out: birds fed the lower dose of the powder, 0.75 percent of the diet, showed a significantly heavier gizzard relative to their body weight than both extract-fed groups and the control. The authors speculate that the fibrous, structural nature of the powdered plant material may have stimulated gizzard development, a phenomenon previously reported with coarse or fiber-rich feed components, but they caution that because particle size was not measured, this interpretation remains speculative.

Blood chemistry offered a few more points of interest. Serum triglycerides were significantly lower in birds receiving 0.75 percent powder, while very-low-density lipoprotein levels were unchanged, suggesting the plant does not exert a broad effect on lipid metabolism. Serum cholesterol was significantly lower in birds receiving both forms of supplementation compared with controls, and markers of kidney function — urea, creatinine, and uric acid — were unaffected, indicating the treatments were not harming the birds. Total protein, albumin, and globulin concentrations also remained stable, painting a picture of animals whose basic metabolic health was intact regardless of diet.

The most intriguing and, frankly, most puzzling findings emerged from the antioxidant measurements. Birds receiving the highest dose of aqueous extract, 1500 milligrams per kilogram, showed a significant increase in serum total antioxidant capacity, a measure of the blood’s non-enzymatic antioxidant potential. That might sound like a win for the plant. But the same group also exhibited significantly elevated serum malondialdehyde, a well-established marker of lipid peroxidation and oxidative damage, alongside significantly reduced glutathione peroxidase activity in the liver, one of the body’s key antioxidant enzymes. In fact, all four supplemented groups showed reduced hepatic glutathione peroxidase activity compared with controls, while liver superoxide dismutase showed only a trend toward reduction and red blood cell enzyme activities were unchanged.

This pattern — higher total antioxidant capacity coexisting with more lipid damage and less enzymatic defense — does not add up to an unequivocal antioxidant benefit, and the authors are careful to say so. Rather, they argue, it points to a complex and potentially pro-oxidant response at the highest extract dose, consistent with the dose-dependent or biphasic effects that phytochemicals sometimes display. It also underscores a broader lesson for the field: antioxidant biomarkers should be interpreted collectively rather than in isolation, and a shift in any single indicator does not necessarily signal improved health. Notably, none of the biochemical changes translated into better growth, feed efficiency, or carcass yield, reinforcing a growing consensus that modulating redox biomarkers under low-stress conditions may not produce tangible production benefits.

The study has honest limitations that shape how its findings should be read. With only four replicate pens per treatment and one bird per pen sampled for biochemical analyses, statistical power to detect subtle effects was limited. The experimental diets were formulated on calculated rather than chemically analyzed nutrient values, and the phytochemical characterization relied on spectrophotometric assays of total phenolics, flavonoids, and coumarins rather than chromatographic identification of individual compounds — meaning the differences between powder and extract cannot be tied to specific active constituents or their bioavailability. The authors also note that under the non-stressed conditions of a well-managed research facility, the birds’ endogenous antioxidant systems may already have been operating near optimal levels, leaving little room for a phytogenic additive to demonstrate measurable gains.

Where does this leave Prangos ferulacea on the crowded shelf of candidate antibiotic alternatives? The study contributes to mounting evidence that phytogenic feed additives can shift oxidative status without necessarily improving performance, particularly in animals that are not under environmental or metabolic stress. The authors chart a clear path forward: comprehensive phytochemical profiling of the plant, formal dose–response studies, investigation of molecular mechanisms such as redox-sensitive signaling pathways like Nrf2, and — perhaps most importantly — testing under oxidative-stress challenge models that better mirror the realities of commercial poultry production. Until then, the mountain herb remains a biochemical curiosity with demonstrated biological activity but, at the doses and conditions tested, no proven ticket to faster-growing, healthier chickens. For an industry under pressure to eliminate antibiotics, that distinction between biochemical activity and production benefit is exactly the kind of hard evidence that keeps the search honest.

Subject of Research: Effects of dietary Prangos ferulacea powder and aqueous extract on growth performance, carcass traits, and antioxidant status in broiler chickens

Article Title: Effects of different levels of Prangos ferulacea (L.) Lindl. (Apiaceae) powder and extract on performance, carcass characteristics, and antioxidant status in broiler chickens

Article References: Janfadah, A., Sadeghi, A. A., & Karimi, A. (2026). Effects of different levels of Prangos ferulacea (L.) Lindl. (Apiaceae) powder and extract on performance, carcass characteristics, and antioxidant status in broiler chickens. Discover Animals, 3(1), Article 98. https://doi.org/10.1007/s44338-026-00250-7

Image Credits: AI Generated

DOI: 10.1007/s44338-026-00250-7

Keywords: Prangos ferulacea, broiler chickens, phytogenic feed additives, antioxidant status, total antioxidant capacity, malondialdehyde, glutathione peroxidase, feed conversion ratio, carcass characteristics, poultry nutrition, antibiotic alternatives, oxidative stress

The research team, based at Ferdowsi University of Mashhad in Iran, worked with 390 male Ross 308 broiler chickens divided into six treatment groups, each with five replicates of 13 birds. The birds were fed either a basal control diet or diets supplemented with a six-strain probiotic containing Lactobacillus acidophilus, Lactobacillus rhamnosus, Pediococcus acidilactici, Bacillus subtilis, Bacillus megaterium and Bacillus amyloliquefaciens at a minimum concentration of one billion colony-forming units per gram, chelated zinc at 120 milligrams per kilogram of feed, chelated copper at 150 milligrams per kilogram, or all three additives combined. To reproduce the conditions under which necrotic enteritis strikes in commercial flocks, the researchers primed the birds with a twenty-fold dose of a coccidiosis vaccine on day 11 — coccidial damage being a classic predisposing factor for the disease — and then administered an aggressive culture of C. perfringens (strain ATCC 13124) at two times ten to the eighth CFU per millilitre on days 13, 14 and 15. The experiment ran to day 21, with growth, carcass traits, gut architecture, microbial populations, blood chemistry, cecal fatty acids, meat oxidation, lesion scores and mortality all measured along the way.

The challenge worked exactly as intended. Birds exposed to C. perfringens grew significantly less than their unchallenged counterparts, finishing the 21-day period at 541 grams of cumulative body weight gain against 584 grams for the clean control group, with feed conversion deteriorating from 1.58 to 1.78 grams of feed per gram of gain. The physiological explanation is well understood: the bacterium produces toxins that erode the intestinal epithelium, triggering inflammation that diverts energy and amino acids away from muscle growth toward immune defence, while the damaged gut lining absorbs nutrients less efficiently. The challenge also left its fingerprints everywhere else in the data — breast muscle yield dropped sharply, ileal lesion scores climbed to 2.80 on a four-point scale, mortality reached 6.15 percent, and meat lipid oxidation, measured as malondialdehyde, rose to 3.10 micrograms per gram.

Against this grim backdrop, the probiotic group emerged as the single most effective intervention. Birds receiving the strain mix on top of the challenge regained nearly all the lost ground, achieving 581 grams of weight gain and posting the best early feed conversion of any challenged group. Under the microscope, the difference was striking: duodenal villus height in the probiotic group reached almost 1600 micrometres, the highest of any treatment and far above the 1121 micrometres seen in challenged, unsupplemented birds, while crypt depth fell and the villus height-to-crypt depth ratio climbed to 8.22 — a classic signature of a healthy, absorptive intestine. The probiotic also reshaped the microbial landscape, cutting ileal C. perfringens counts from 14 million to 5.5 million CFU per gram and boosting resident Bacillus populations, the very organisms best known for producing antibacterial compounds such as lichenicidin that punch holes in pathogenic cell membranes.

Chelated zinc told a complementary story. Zinc-supplemented challenged birds matched the probiotic group in body weight, and their feed intake over the full rearing period was the highest of any treatment at 985 grams. The mineral’s benefits likely stem from its well-documented role in tightening the intestinal barrier and modulating inflammation: earlier work cited by the team shows chelated zinc upregulates the anti-inflammatory cytokine IL-10 while suppressing IL-8 and other pro-inflammatory signals, restoring intestinal cell membrane integrity during infection. Zinc’s superior performance relative to inorganic sources is usually attributed to the higher bioavailability of chelated forms, which are absorbed through different pathways and place less demand on plasma albumin for transport. Ileal lesion scores in the zinc group fell to 1.60, and lipid oxidation in thigh meat dropped to 2.65 micrograms per gram, reflecting zinc’s participation in the bird’s antioxidant machinery.

Copper, by contrast, was the weakest solo performer. Birds given chelated copper grew no better than the unsupplemented challenge group over the full period and actually showed the lowest early body weight of all treatments. Yet copper was not without value: challenged birds receiving it recovered breast muscle yield to 18.53 percent of live weight, essentially matching the unchallenged control, and mortality fell to 1.53 percent. The authors note that copper’s antibacterial reputation rests largely on pharmacological doses around 250 milligrams per kilogram, considerably above the 150 milligrams per kilogram used here, which may explain the muted growth response.

The triple combination produced a genuinely mixed verdict. On several fronts it excelled: birds receiving probiotics, zinc and copper together suffered zero mortality, scored the lowest ileal lesion severity of any challenged group at 1.40, restored breast yield to 18.92 percent, and preserved jejunum architecture so well that their villus height-to-crypt depth ratio of 7.68 rivalled the healthy control. Blood biochemistry also shifted, with the combination group showing the lowest serum glucose and HDL cholesterol, consistent with altered lipid and metal metabolism when both minerals arrive in organic complexes. However, the trio failed to replicate the probiotic’s standout gains in body weight and duodenal villus height, and it delivered only intermediate results for feed intake.

The cecal short-chain fatty acid data reveal why more is not always better. Probiotic supplementation raised acetate, propionate and butyrate concentrations toward or above control levels — butyrate being the preferred fuel of enterocytes and a critical reinforcement agent for tight junctions. Zinc and copper given alone, however, sharply suppressed the fatty acid profile, with acetate falling to 25.56 and 22.50 micrograms per gram respectively. This suppression is thought to reflect the sensitivity of Lactobacillus species, key fatty-acid producers, to elevated concentrations of both metals, with copper reported in prior studies to eliminate beneficial strains such as Lactobacillus johnsonii outright. The combination group, containing the probiotic, largely avoided this pitfall, posting acetate and butyrate values statistically comparable to the control — evidence that the live microbes could partially buffer the antibacterial pressure of the minerals on the fermentative community.

The study’s overall picture is nuanced rather than triumphalist. C. perfringens unquestionably devastates growth, gut morphology, meat quality and survival, and probiotic supplementation stands out as the most consistently protective single intervention, working through competitive exclusion, organic acid production, bacteriocin release and direct architectural repair of the villi. Zinc earns its place as a robust second pillar, particularly for feed intake and barrier integrity, while copper contributes to meat yield and survival but underperforms at the dose tested. The three-way combination shines where it matters most to producers — mortality, lesion severity and breast yield — but dilutes some of the probiotic’s growth-promoting power, possibly through mineral-driven suppression of the very bacteria that make probiotics work. For an industry searching for antibiotic alternatives, the message is that nutritional strategies must be designed with their interactions in mind: the goal is not simply to stack protective additives, but to balance their antimicrobial potency against their capacity to nurture the beneficial fermenters that keep the gut — and the flock — thriving.

Subject of Research: The effects of multi-strain probiotics, chelated zinc and chelated copper on broiler chickens challenged with Clostridium perfringens.

Article Title: The Effect of Multi‐Strain Probiotics, Zinc and Copper on the Performance of Broiler Chickens Challenged With Clostridium perfringens

Article References: Kazemi, A., Kermanshahi, H., Heravi, R. M., Jouzani, G. S., & Javadmanesh, A. (2026). The Effect of Multi‐Strain Probiotics, Zinc and Copper on the Performance of Broiler Chickens Challenged With Clostridium perfringens. Veterinary Medicine and Science, 12(5), Article e71176. https://doi.org/10.1002/vms3.71176

Image Credits: AI Generated

DOI: 10.1002/vms3.71176

Keywords: necrotic enteritis, Clostridium perfringens, broiler chickens, probiotics, zinc supplementation, copper supplementation, gut health, intestinal microbiota, short-chain fatty acids, poultry nutrition, antibiotic alternatives, feed conversion ratio