The Kadaknath chicken has high meat value owing to its superior nutritional quality, characterized by high protein content, low fat levels and a favorable fatty acid composition (Deori et al., 2025). Furthermore, the meat shows higher antioxidant capacity compared to that of commercial broilers (Sehrawat et al., 2021). In addition, the birds exhibit strong disease resistance, as indicated by higher cytokine gene expression and a more robust mucosal immune response (Thakur et al., 2020). Fatty Liver Hemorrhagic Syndrome (FLHS) is one of the most important non-infectious metabolic disorders affecting laying hens globally. It is characterized by accumulation of excessive lipid accumulation (hepatic lipidosis) within the liver, leading to increase its fragility, spontaneous rupture, massive intra-abdominal hemorrhage and sudden death (Shini et al., 2009; Trott et al., 2014). The syndrome poses a serious threat to economic sustainability and welfare because it results in significant losses in egg production and quality as well as direct mortality, which can reach up to 5% during a laying cycle (Julian, 2005; Shini et al., 2019). The economic impact is further magnified in intensive production systems where the prevalence of FLHS is highest.
       
The pathogenesis of FLHS is complex. It involves complex interaction of nutritional, genetic, environmental and hormonal factors. This initiate with imbalance in hepatic lipid metabolism, where the rate of lipid synthesis and deposition exceeds the liver’s capacity for lipid oxidation (Squires and Leeson, 1988; Walzem et al., 1993; Gao et al., 2019; Shini et al., 2020). This imbalance is caused by a persistent positive energy balance, where hens consume more dietary energy for their requirements like maintenance and egg production. The surplus energy is converted to triglycerides and stored in the liver that leads into hepatocyte distension and steatosis (Butler, 1976; Leeson, 2007). This pathological fat infiltration weakens the hepatic architecture particularly the reticulin framework that provides structural support to the sinusoids. This causes condition known as reticulolysis (Hall, 1974; Trott et al., 2014). The loss of liver structural integrity may leads to rupture, often triggered by minor trauma or physiological stress, resulting in fatal hemorrhage (Trott et al., 2014; Yang et al., 2017; Zhu et al., 2021).
       
Poultry housing systems play critical role in the incidence of FLHS. Several studies have consistently shown that hens kept in conventional cage systems exhibit a significantly higher prevalence of FLHS as compared to those in free-range setups (Weitzenburger et al., 2005; Shini et al., 2019). The restricted mobility of caged hens is the main cause of this discrepancy which lowers their maintenance energy requirements and promotes obesity (Shini et al., 2019). Moreover, the liver is severely strain by the metabolic demands of high egg production, a trait that is heavily selected for in contemporary commercial strains (Meng et al., 2021; You et al., 2023). Estrogen, which stimulates hepatic lipogenesis at the start of the laying period for yolk component lipids, increases the liver burden and risk of FLHS (Polin and Wolford, 1976; Pearson and Butler, 1978). This combination of genetic predisposition for high yield, high-energy diets and limited physical activity creates a “perfect storm” for the development of the syndrome in caged layers.
       
Furthermore, there is evidence that environmental stress, particularly heat stress may play a major role in FLHS outbreaks. If feed intake is not appropriately adjusted, higher ambient temperatures effectively create a more positive energy balance by lowering the bird’s energy requirements for thermoregulation (Ivy and Nesheim, 1973, Wasti et al., 2020). Many investigations indicate that the incidence of FLHS exhibits a seasonal pattern, peaking in the warmer spring and summer months (Trott et al., 2014).  The metabolic disorder may also be exacerbated by nutritional imbalances or deficiencies. Lipidosis is accelerated by diets lacking in lipotropic agents like choline, methionine, vitamin E and vitamin B12. These agents hinder the liver’s capacity to mobilize fat (Squires and Leeson, 1988). Liver damage and an increased risk of bleeding have also been associated with the presence of mycotoxins, such as aflatoxins, or specific dietary components, such as rapeseed meal (Bryden et al., 1979; Bhatnagar et al., 1980).
       
Despite extensive research in commercial hybrid layers like the Isa Brown and Hy-Line Brown, there is a noticeable lack of research on FLHS in native or indigenous breeds like the Kadaknath. The Kadaknath is an Indian meat breed well known for its resilience and black meat which is now increasingly integrated into semi-intensive and intensive production to satisfy specific market needs. Its unique genetics, possible variable metabolic rates and adjustment to local conditions can influence its possible susceptibility or resistance to metabolic disorders such as FLHS. Investigating the pathology and epidemiological pattern of FLHS in this breed is essential to develop targeted prevention and control measures for FLHS that can guarantee the breed’s productivity and welfare. Hence, this study was intended to systematically evaluate the mortality pattern and pathology of Fatty Liver Hemorrhagic Syndrome in Kadaknath flocks. Further the specific breed level manifestations and associated risk factors pertaining to FLHS was determined through the integration of gross and histopathological findings with annual mortality data. This would aid to the poultry veterinarians and Kadaknath chicken farmers to manage the health of their flocks and help in the sustainable management of this breed.

The present study was carried out from January 2022 to December 2024 in the Department of Veterinary Pathology, College of Veterinary Science and Animal Husbandry, NDVSU, Rewa (M.P.), with the objective of investigating the prevalence and pathological features of Fatty Liver Hemorrhagic Syndrome in Kadaknath chickens reared under different management systems. There are two types of poultry farming in Rewa district. On the one hand, backyard poultry farming continues to be a significant source of income for rural households with smaller flocks, while organized commercial layer farms run on semi-intensive or intensive systems with flock sizes frequently exceeding several hundred birds. Because of its cultural and economic significance, the Kadaknath breed-which is distinguished by its black plumage, black meat and ability to adapt to harsh environments-has been raised more frequently in both systems.
 
Study period
 
The study was carried out over three consecutive years, from January 2022 to December 2024, with the intention of collect the seasonal influences and the effect of production cycles on the occurrence of FLHS. Throughout the study period birds were collected from different locations of Rewa district from both organized commercial and backyard farm. A total of 830 Kadaknath layer birds (organized farm birds n=630; backyard farms birds n=173) were examined. Birds from organized farms were reared under standard conditions with maize-soybean-based rations, mineral and vitamin supplementation and vaccination programs recommended for commercial layers or sometimes commercially available feed. Birds from backyard flocks were typically reared under scavenging conditions and supplemented with household grains such as maize, wheat and kitchen leftovers, with limited preventive healthcare measures.
 
Categorization birds
 
The birds examined in the present study represented a range of ages and production stages. The birds were divided into four groups based on data gathered from farm records and poultry keepers: pre-laying pullets (n=93), which were 18 to 20 weeks old, early layers (n=187), which were 21 to 30 weeks old, peak layers (n=280), which were between 31 and 50 weeks old and late layers (n=270), which were older than 50 weeks, when egg production typically starts to decrease. This classification was considered as an important to evaluate the relationship between age, production stage and the occurrence of FLHS lesions. Birds that had either unexpectedly died on farms, displayed clinical indicators of FLHS, such as a sudden decrease in egg production, pale combs, or unexpected mortality were all included in the study. A pre-made proforma was used to record data on the flock’s size, management system, feeding habits, vaccination schedules, egg production performance, mortality rate and incidence of unexpected deaths. Discussion with farm owners and poultry keepers were also conducted to collect detailed history of feed composition, seasonal stress and management practices.
 
Postmortem examination
 
Necropsy was carried out for all 830 birds by standard post-mortem procedure. Each bird underwent a thorough internal and external examination. External examination included observation of general body condition, plumage, coloration of comb and wattles and any signs of hemorrhage. All visceral organs were thoroughly examined during the internal examination, with the liver and surrounding structures receiving particular attention. Gross lesions were recorded on the spot in descriptive form.
       
For histopathological evaluation, representative samples of liver was collected from both affected and unaffected birds. Collected tissue samples were fixed in ten percent neutral buffered formalin immediately. The fixed tissues were processed using standard paraffin embedding techniques, sectioned at five micron thickness using a rotary microtome and stained with hematoxylin and eosin for histological examination. Histological observations focused for particularly hepatic changes, for examples hemorrhages, sinusoidal congestion, necrosis and parenchymal disorganization. To estimate FLHS prevalence in the sampled Kadaknath layers, data were compiled and analyzed using descriptive statistics. Lesion occurrence was recorded agewise, season wise and according to production stage to identify patterns of increased susceptibility.

In this study total 830 dead Kadaknath layer birds were collected from backyards and organized farm in and around Rewa district. A total of 830 birds were examined across different laying stages, of which 105 were affected with FLHS. As shown in Fig 1, the pre-laying stage (18-20 weeks), 93 birds were examined and 5 were affected, while during the early laying stage (21-30 weeks), 187 birds were examined with 34 affected cases. At the peak laying stage (31-50 weeks), 280 birds were examined and 30 were affected, whereas in the late laying stage (>50 weeks), 270 birds were examined and 24 were affected. The prevalence calculated for FLHS was 12.65. The layers which were in 21 and 30 weeks of production age had shown highest prevalence of FLHS, which corresponding to the early phase of egg production. In this early laying group, 18.2 per cent of examined birds were affected with FLHS which was significantly higher than the peak layers, late layers, or pre-laying pullets. The peak laying birds between 31 and 50 weeks of age showed a prevalence of 10.7 per cent, while late layers beyond 50 weeks exhibited 8.9 per cent prevalence. The pre-laying group recorded the lowest prevalence at 5.4 per cent. These findings suggest that the early laying birds were more susceptible to FLHS condition than birds in other production stages. This trend aligns with earlier reports that the onset of egg production, accompanied by surges in circulating estrogen and heightened hepatic lipogenesis, predisposes hens to fat accumulation and vascular fragility (Polin and Wolford, 1976; Pearson and Butler, 1978).


       
As described in Fig 2, seasonal distribution showed that the FLHS cases were observed more commonly during the winter months. Season wise, winter accounted for 19.2 per cent of all diagnosed cases. This is followed by summer with 10.6 per cent and then last rainy season with 9.3 per cent. The higher winter prevalence contrasts with earlier studies that emphasized spring-summer peaks in other regions (Trott et al., 2014). This difference may reflect local feeding practices, management systems, or climatic stressors unique to Rewa district. Importantly, the consistent association of FLHS with periods of metabolic or environmental stress underscores its multifactorial etiology (Shini, 2014).


       
During the three-year investigation in and around Rewa district, clinical signs preceding mortality were subtle. Most affected Kadaknath layers seemed to be normal until they suddenly collapse and died. These indicate the peracute nature of fatty liver hemorrhagic syndrome (FLHS). In a subset of cases, farm records and observations recorded the pale combs, reduced egg production and occasional lethargy, but these sings were nonspecific. The peracute onset reflects the underlying mechanism of hepatic rupture and acute intracoelomic hemorrhage, which provides little time for outward clinical manifestation (Crespo and Shivaprasad, 2003; Julian, 2005).
       
Necropsy examination provided striking gross lesions, conclusive evidence for Fatty Liver Hemorrhagic Syndrome (FLHS). A prominent and consistent finding was excessive fat deposition within the coelomic cavity (Fig 3A), particularly surrounding the proventriculus, gizzard and on breast muscle. In many cases there was increased coronary fat around the heart (Fig 3B) which supporting the role of positive energy balance and restricted mobility in predisposing birds to the syndrome (Butler, 1976; Leeson and Summers, 1995). The fat deposition was prominent on gizzard compared to other abdominal organs (Fig 3C). The most significant lesions were observed in the liver. The liver lobes were markedly enlarged, with a pale yellow to orange-tan discoloration and had a soft (Fig 3D), friable consistency, often breaking apart upon gentle handling. The hepatic capsule was frequently disrupted by multiple subcapsular hematomas and pinpoint petechial or larger ecchymotic hemorrhages (Fig 3D). In severe cases, rupture of the liver (Fig 4A) was evident leading to large organized blood clots (Fig 4B) within the abdominal cavity (hemoabdomen; Fig 4C). The liver lobes border lost its sharpness became round. The rupture of liver might be due to reticulin breakdown weakening the hepatic scaffolding and predisposing the tissue to rupture (Hall, 1974). The ovarian follicles often appeared hemorrhagic and degenerated (Fig 4D), with some cases showing ruptured egg material, suggesting a systemic metabolic failure affecting the reproductive tract. Sometimes well formed egg was found in reproductive tract (Fig 4D satellite). These findings corroborate the hallmark features of the syndrome described in earlier studies (Dinev, 2010; Shini et al., 2019).




       
Interestingly, the prevalence of lesions was highest in early layers, a stage when birds transition to peak production and hepatic lipid metabolism is most active. This suggests that the combination of high estrogenic drive, rapid hepatic lipid synthesis and structural vulnerability culminates in gross hepatic failure (Walzem et al., 1999). Seasonal variation in gross lesions, particularly their higher frequency in winter, may be linked to changes in feed intake and energy metabolism in response to colder conditions, although further metabolic studies would be needed to confirm this hypothesis.
       
Histopathological analysis of affected livers demonstrated minor vacuolar degeneration of hepatocytes along with large scale hemorrhage. Hepatocytes were swollen with clear cytoplasmic vacuoles displacing nuclei, indicating fat accumulation (Fig 5A and 5B). These findings are typical of hepatic steatosis and have been documented in both experimental estrogen-induced models and field cases (Shini, 2014). Sinusoidal congestion and multifocal hemorrhages were evident within the parenchyma (Fig 5C). In some sections, larger hemorrhagic foci coalesced into haematomas, supporting the gross finding of hepatic rupture. The histopathological distinction between simple hepatic steatosis and FLHS was also evident. While steatosis involves fat-laden hepatocytes without mortality, FLHS is characterized by fatty change in combination with parenchymal hemorrhage and vascular compromise, explaining its acute fatal outcomes (Diaz et al., 1994).


       
From a management perspective, these findings reinforce the need for preventive strategies including dietary energy control, supplementation with lipotropic agents and minimizing environmental stressors. In the case of Kadaknath chickens, adaptation to semi-intensive and backyard systems may offer some protection compared to intensive cage housing, but the observed prevalence underscores that the breed is not inherently resistant. Tailored strategies are therefore essential to safeguard both productivity and welfare in indigenous and commercial flocks alike.

The present investigation confirms that Fatty Liver Hemorrhagic Syndrome (FLHS) is a significant metabolic disease that affect Kadaknath chickens especially during early laying stage. Even this tough native breed is affected with 12.65% prevalence rate. The prevalence of the disease during winter and birds under high control conditions underlines the role of environmental and nutritional factors on the disease. Typical hepatic lipidosis and hemorrhage was confirmed by both gross and histopathologic results. In order to improve the flock’s health and productivity, prevention should focus on reducing metabolic and environmental stress, promoting healthy nutrition and combining lipotropic substances.

This work was supported by Department of veterinary Pathology, College of Veterinary Science and A.H, NDVSU, Rewa, M.P., India.

All authors declare that they have no conflict of interest.