Descriptive epidemiology of spotty liver disease in Australian cage-free brown egg layer chicken flocks with a scratch area.

Spotty Liver Disease (SLD), caused by Campylobacter hepaticus or C. bilis infection in adult female chickens continues to emerge as a major disease problem in cage-free production systems. Free range production has become the predominant system in Australian egg production and SLD is widespread in these farms. Previous studies have identified having a scratch area as a key determinant for SLD occurrence. An Australia-wide survey of egg production flocks with scratch areas was conducted regarding SLD including 48 individual flocks. Descriptive information on the facilities and flock management practices was reported. The incidence of SLD, age of first outbreak, initial mortality rate, duration of elevated mortality, and magnitude and duration of any associated egg production decline are described. Recurrence of SLD in the same flock was also reported and discussed. Therapies applied were recorded and assessed across SLD severity and duration. SLD occurred in 66.7% of layer flocks whose facility included a scratch area. Recurrent SLD outbreaks occurred in 31% of flocks experiencing SLD. Antibiotic medication reduced duration of mortality and egg production decline. Antibiotic therapy was associated with reduced duration of mortality and a less severe and shorter duration of egg production drops compared to untreated flocks. PCR detection of C. hepaticus in cloacal swabs and house dust samples and a serological ELISA test were compared and evaluated as diagnostic aids or as possible predictors of SLD outbreaks. The ELISA showed substantial agreement with detection of C. hepaticus in cloacal swabs by PCR. Examining composite house dust samples by PCR for C. hepaticus DNA appeared to be the most convenient and cost-effective aid to diagnosis and as a putative predictor for SLD outbreaks.

Perceptions of Sheep Farmers and District Veterinarians towards Sheep Disease Management in New South Wales, Australia.

The study objectives were to understand the practices and perceptions of sheep farmers and district veterinarians (DVs) towards sheep health management and, the impact of disease at the farm level in addition to the availability, accessibility, and use of veterinary services. Data were collected using question-based surveys, distributed online and in-person to sheep farmers (45 respondents) and DVs (25 respondents). Most farmers were male, ≥51 years old, who placed a high priority on the health and welfare of their sheep. For disease prevention most farmers vaccinated their sheep (91%) and 86.7% had a farm biosecurity plan, although its components and their application varied, e.g., the isolation of new or sick sheep. Fencing costs were most frequently identified (70.5% respondents) as a financial concern for sheep farmers. Their most common sources of information about disease control and prevention were DVs (66.7%), private veterinarians (60.0%), the internet (42.9%), rural suppliers (35.7%), and farmers/neighbours (28.6%). Fifty-eight percent of farmers reported a long distance from veterinarian services. Farmers preferred to receive information via email (77.8%), whereas 56% of DVs preferred to share information via phone call. This discrepancy presents an opportunity to align these mechanisms more closely for effective dissemination of information and increased producer engagement.

Identification of epidemiological risk factors for spotty liver disease in cage-free layer flocks in houses with fully slatted flooring in Australia.

Spotty liver disease (SLD) is recognized to be caused by infection with Campylobacter hepaticus in adult layer hens farmed in cage-free environments. SLD is an emerging disease as cage-free egg production increases in popularity in response to desires for improved welfare of poultry. Outbreaks of SLD are frequently experienced around peak egg production in flocks, commonly between 25 and 40 wk of age. The disease becomes manifest with increased exposure and access of the birds to the feces of the flock. This study follows from a previous epidemiological survey of free-range and barn flocks in Australia which identified the presence of a scratch area within the laying house as a major risk factor for the occurrence of SLD. However, that survey also observed SLD occurrence in 45% of houses with a fully slatted floor (no scratch area). The present study describes a further analytical survey aimed at identification of risk factors for SLD in houses with fully slatted flooring. A comprehensive questionnaire was completed for 49 cage-free flocks from point of lay until 40 wk of age across Australia, retrieving information on house design, bird breed, flock size, stocking densities, bird growth, and performance and the occurrence of SLD. Multiple logistic regression model building was used to separate factors and identify important management factors that may be amenable to modify the occurrence of SLD in egg layers. Key determinants of SLD identified from the analyses were that houses with mechanical ventilation (such as tunnel ventilation) have some protection from SLD and an increase of an extra 1 bird/m2 of nest space increased odds of occurrence of SLD by 1.172 times. A recommendation to not exceed 112 brown egg layer hens/m2 of nest space in naturally ventilated houses with a full slat floor was suggested. A delay in birds reaching 60% hen day production (HD) by 1 wk is suggested as a possible predictor for a subsequent outbreak of SLD.

Scratch area as an epidemiological risk factor for Spotty Liver Disease in cage-free layers in Australia.

Spotty Liver Disease (SLD) is a serious problem in laying hens farmed in cage-free systems. The causative organism, Campylobacter hepaticus, is regarded as having a fecal-oral method of transmission and hence may build up and spread readily in housing systems which allow ease of direct contact of hens with the flock's fecal material. The epidemiology of SLD has not been thoroughly investigated. An initial cross-sectional analytical epidemiological survey of SLD in free range and barn layer systems was conducted in Australia over 2019 to 2021.The survey involved rearing flocks (n = 32) which were then followed through into laying flocks (n = 24) up to 40 wk of age. Cloacal swabs were collected during rearing and lay for C. hepaticus detection by PCR. Flocks were classified as "Cases" (n = 18) where clinical SLD according to the case definition was observed or "Controls" (n = 6) which were clinically unaffected. No C. hepaticus was detected in cloacal swabs from rearing houses whereas the organism was detected in 18 Case flocks in lay and from 2 Control flocks in lay. All layer houses that incorporated a scratch area (n = 13) were categorized as Cases. Thus, having a scratch area is a key determinant for SLD and no analyses of further contributory factors from these flocks were able to be made. Of the remaining 11 flocks which had floors fully covered by slats, 5 were Cases (45%). Further risk factor analysis was compromised by this small sample size and identification of other significant associations was not possible. A larger survey investigating flocks laying in houses with fully slatted floors was undertaken to further the understanding of SLD epidemiology and is reported in a companion paper.

An evaluation of bird weight and diet nutrient density during early lay on ISA Brown performance, egg quality, bone characteristics, and liver health at 50 weeks of age.

This study compared the impact of a higher nutrient density (HND) or lower nutrient density (LND) diet fed during early lay to either heavier weight (HW) or lighter weight (LW) ISA Brown hens. At 18 wk of age (WOA) pullets (n = 240) were evenly assigned to either HW (n = 120) or LW (n = 120). Sixty birds from each weight group were then randomized to either the HND or LND diet treatments which were fed from 18 to 24 WOA inclusive. At 25 WOA the LND diet replaced the HND diet. All hens remained on LND diet to 50 WOA. Hen performance was measured from 18 to 50 WOA. Femur and liver health were evaluated at 50 WOA. Egg quality was assessed from 46 to 50 WOA. The 18 WOA HW hens had higher BW, cumulative egg production, cumulative feed intake (CFI), and cumulative egg mass (CEM) to both 24 and 50 WOA (P < 0.01). At 24 WOA the HND diet also generated higher BW (P < 0.001), CEM (P < 0.001) and lower cumulative feed conversion ratio (CFCR) (P < 0.01), the latter being sustained to 50 WOA (P < 0.01). At 50 WOA CFCR of LW birds was lower than HW birds (P < 0.01). Egg weight (EW), yolk diameter, and percent yolk weight were higher (P < 0.05) in the HW birds with the highest albumen to yolk ratio in LW birds (P < 0.05). Egg shape index was higher in LND diet fed birds (P < 0.01) while LW hens had higher shell phosphorus (P < 0.05). Body weight and diet nutrient density interacted on femoral diameter and cortical thickness being higher (P < 0.01) in LW birds fed HND than LW birds fed LND diets. Fatty liver hemorrhagic scores (P < 0.05) and liver lipid peroxidase (P < 0.001) at 50 WOA were higher in HW and LND diet treatments. Concurrently HW birds had the highest CFI and EW while CFCR and liver health were superior in LW and the HND diet treatment.

A meta-analysis of experiments linking incubation conditions with subsequent leg weakness in broiler chickens.

A series of incubation and broiler growth studies were conducted using one strain of broiler chicken (fast feathering dam line) observing incubation effects on femoral bone ash % at hatch and the ability of the bird to remain standing at 6 weeks of age (Latency-To-Lie). Egg shell temperatures during incubation were consistently recorded. Parsimonious models were developed across eight studies using stepwise multiple linear regression of egg shell temperatures over 3-day periods and both bone ash at hatch and Latency-To-Lie. A model for bone ash at hatch explained 70% of the variation in this factor and revealed an association with lower egg shell temperatures during days 4-6 and 13-15 and higher egg shell temperatures during days 16-18 of incubation. Bone ash at hatch and subsequent Latency-To-Lie were positively correlated (r = 0.57, P<0.05). A model described 66% of the variation Latency-To-Lie showing significant association of the interaction of femoral ash at hatch and lower average egg shell temperatures over the first 15 days of incubation. Lower egg shell temperature in the early to mid incubation process (days 1-15) and higher egg shell temperatures at a later stage (days 16-18) will both tend to delay the hatch time of incubating eggs. Incubation profiles that resulted in later hatching chicks produced birds which could remain standing for a longer time at 6 weeks of age. This supports a contention that the effects of incubation observed in many studies may in fact relate more to earlier hatching and longer sojourn of the hatched chick in the final stage incubator. The implication of these outcomes are that the optimum egg shell temperature during incubation for broiler leg strength development may be lower than that regarded as ideal (37.8°C) for maximum hatchability and chick growth.

Dietary supplementation with vitamin E modulates avian intestinal immunity.

The effect of dietary vitamin E on immunoglobulin A (IgA) antibody production, which acts as the first line of defence at the intestinal mucosa, has not been evaluated in chickens. In the present study the impact of the inclusion of supplementary levels of vitamin E to the diet, on total and antigen-specific IgA antibody titres, T-cell subsets and Ia+ cells, was assessed. From hatching, chickens received a maize-based diet which was supplemented with either 25, 250, 2500 or 5000 mg dl-alpha-tocopherol acetate/kg. Primary immunisation with tetanus toxoid (T. toxoid) emulsified in a vegetable oil-in-water adjuvant was administered by the intraperitoneal route at 21 d of age. At 35 d of age all birds received an oral booster vaccination of T. toxoid. Significantly higher total IgA antibody titres were present in the day 42 intestinal scrapings of birds receiving the 5000 mg/kg vitamin E-supplemented diet (VESD) (P=0.05) and a notable increase was observed in birds receiving the 250 mg/kg VESD (P=0.06). At days 21 and 42 total serum IgA antibody titres of birds receiving the 250 mg/kg VESD was significantly higher (P<0.05) than the control birds. Following immunisation with T. toxoid, birds receiving the 250 and the 5000 mg/kg VESD had elevated anti-T. toxoid IgA antibody titres in final day intestinal scrapings, which, for the latter group was statistically significant (P=0.02). Both of these groups also demonstrated increased titres of anti-T. toxoid IgA in the serum at day 42. Birds receiving the 250 mg/kg VESD exhibited a notable increase in the percentage of T-helper cells and Ia+ cells in peripheral blood on day 26. The results illustrate the potential for some levels of dietary vitamin E supplementation to act as an immunomodulator of total and antigen-specific IgA antibody.