Developing a selective culturing approach for Campylobacter hepaticus.

Campylobacter hepaticus, the causative agent of Spotty Liver Disease (SLD) is an important disease in cage-free egg producing chickens causing mortality and production drops. C. hepaticus is a slow growing Campylobacter easily overgrown by fecal bacteria. It is currently only reliably isolatable from bile samples. A selective media for isolation from feces or environment would assist diagnosis and impact assessment. Growth of five Australian C. hepaticus isolates was studied using Horse blood agar (HBA), sheep blood agar (SBA), Bolton, Preston and Brain Heart Infusion (BHI) base media. Blood and/or bile were added to Bolton, Preston and BHI medias. C. jejuni was used as a positive control. Plates were incubated in duplicate under microaerophilic conditions at 42°C for 10 days and examined at days 3-5 and 7-10 of incubation. Each isolate was examined for sensitivity to 14 antimicrobials using HBA sensitivity plates. Growth was inhibited by BHI and by added bile, while blood improved growth. Further replicates using SBA, HBA, Bolton and Preston media showed best growth on Bolton agar with blood. All five C. hepaticus isolates were resistant to trimethoprim and vancomycin, while four were also resistant to rifampicin and bacitracin. Media based upon Bolton plus blood supplemented with vancomycin and trimethoprim might be used as the most appropriate media for selective growth of C. hepaticus. The addition of bile to media for C. hepaticus isolation and growth will inhibit growth and is not advised.

Association of feed efficiency with organ characteristics and fatty liver haemorrhagic syndrome in laying hens.

Poor feed efficiency (FE) in hens impacts body weight (BW) and may reflect suboptimal health. Fatty Liver Haemorrhagic Syndrome (FLHS) is mostly observed in laying hens and affects egg production and hen performance. The aim of this study was to investigate the relationships of FE and BW with organ characteristics, liver composition and incidence of FLHS of 150 individually housed ISA Brown hens ranked on the basis of feed conversion ratio (FCR) attained from early lay. At 45 weeks, 10 birds per FE group (HFE-High feed efficient; MFE-medium feed efficient; LFE-low feed efficient) were randomly selected and euthanized. Hen BW was positively associated with feed intake and FCR. The HFE hens had a lower abdominal fat pad and liver weight compared to LFE hens. FLHS lesion score was higher (worse) in the LFE than HFE hen group and was moderately positively associated with BW and abdominal fat pad, but strongly positively associated with liver weight. Liver pathology of LFE hens showed hepatocytes with abnormal retention of lipids causing distended cytoplasmic vacuoles compared to the HFE hens. Hens which exhibited poorer FE in early lay had heavier abdominal fat pads, heavier, fatter livers and were more prone to FLHS.

The role of hen body weight and diet nutrient density in an extended laying cycle.

The egg production (EP), egg quality and health of heavier or lighter hens fed a diet of either higher nutrient density (HND) or lower nutrient density (LND) during early lay, was assessed at very late lay. Based on their body weight (BW) at 18 wk of age (WOA) ISA Brown pullets were allocated as either heavier weight (HW; average 1.65 kg) or lighter weight (LW: average 1.49 kg). Half of each BW group received the HND (2,901 kcal/kg; 17.6% crude protein (CP) or LND (2726 kcal/kg, 16.4% CP) diet from 18 to 24 WOA. From 25 to 90 WOA all birds received identical early, then mid and late-lay diets. Hen BW was measured after peak-lay (36 WOA) and at 90 WOA. At 89 WOA and across 18 to 36 and 18 to 89 WOA feed intake (FI), EP, egg mass (EM), and feed conversion ratio (FCR) were calculated. Eggshell quality, breast score, relative ovary weight and liver and bone health were evaluated in very late lay. Differences in BW continued to 90 WOA. At 36 WOA HW hens produced heavier eggs, and had higher 18 to 36 WOA cumulative FI, EM (P < 0.001) and FCR (P < 0.05). When 89 WOA HW birds consumed more feed (P < 0.001) but EP, EM and FCR did not differ from LW hens. Cumulatively, 18 to 89 WOA FI and EM were higher for HW hens (P < 0.05), but cumulative EP and FCR was not different. The early-lay HND diet improved very late lay eggshell thickness (P < 0.05) and shell breaking strength (P = 0.05). Lighter hens fed HND and HW hens fed LND diet produced heavier eggs, higher relative oviduct weight and lower liver lipid peroxidase in very late lay (P < 0.05). Bone strength did not differ, but LW hens had higher femoral manganese and zinc (P < 0.05), lowering their likelihood of osteoporosis. Overall LW hens sustained EP throughout a longer laying cycle with beneficial bone characteristics. The HND diet improved eggshell strength and, in LW hens reduced hepatic oxidation.

The influence of hen size and diet nutrient density in early lay on hen performance, egg quality, and hen health in late lay.

The effect of hen size and diet nutrient density during early lay on egg production (EP) at 24 and 69 wk of age (WOA) and late lay egg quality and hen health was evaluated. Based on bodyweight (BW) at 18 WOA ISA Brown hens were assigned as heavier (HW; n = 120) or lighter weight (LW; n =120). Sixty birds from each BW group were fed an early-lay diet of higher nutrient density (HND), or lower nutrient density (LND) between 18 and 24 WOA. From 25 WOA all hens received the same early-lay diet and then from 40 WOA the mid-lay diet. Hen average daily feed intake (ADFI), hen-day EP, egg weight (EW), egg mass (EM), and feed conversion ratio (FCR) were assessed at 24 and 69 WOA. Between 66 and 70 WOA eggshell and internal egg quality was evaluated and at 70 WOA BW, liver and bone health were assessed. At 24 WOA BW was highest in HW birds and birds receiving the HND diet (P < 0.01). Concurrently ADFI, and FCR were higher and hen-day EP was lower in HW compared to LW birds (P < 0.05). The HND diet resulted in lower ADFI and FCR at 24 WOA, but higher EW and EM compared to the LND diet (P < 0.01). At 69 WOA HW birds had higher ADFI, EW (P < 0.02) and heavier 70 WOA BW compared to LW hens. The lower FCR of the LW birds at 69 WOA was approaching significance (P = 0.054). Hen weight and diet density did not affect 69 WOA egg production. Between 18 and 69 WOA cumulative FI and EM were higher in HW hens (P < 0.01) than LW hens, as was cumulative FCR (P = 0.053). Hen weight and diet density did not alter 66-70 WOA internal egg quality, but the HND diet generated thicker eggshells and higher eggshell breaking strength (P < 0.05). Seventy WOA liver health, keel curvature and femur breaking strength did not differ. Overall LW hens had lower FCR than HW hens and the early-lay HND diet facilitated improved eggshell integrity during late lay compared to the LND diet.

Spotty Liver Disease: A review of an ongoing challenge in commercial free-range egg production.

Spotty Liver Disease is an acute infectious disease of layer chickens that was likely first described in the USA and Canada in the 1950s and 1960's. The disease occurs almost exclusively in barn and free-range production systems. Outbreaks usually, but not exclusively occur in young layers (≅25 weeks) at peak of lay. Indicators of SLD include an acute drop in egg production of up to 35%, together with increased mortality of up to 15%. A presumptive diagnosis at post mortem is made with the detection of characteristic small yellow-white necrotic hepatic lesions, together with a fibrinous peri-hepatitis, excess pericardial and peritoneal fluid, and usually enteritis with diarrhoea. Histopathology reveals a multifocal acute hepatocellular necrosis with fibrin and occasional haemorrhage. Control measures trialled include use of antibiotics, improved biosecurity and hygiene, as well as management practices directed at reducing stress in flocks. However, none other than treatment with antibiotics has been consistently effective which suggested a bacterial aetiology. In 2015, a novel fastidious thermophilic, microaerobic campylobacter was isolated from symptomatic SLD flocks in the UK. Subsequently, an Australian group isolated and further characterised a genetically similar bacterium and named it Campylobacter hepaticus. The bacterium can be cultured from the liver and bile of infected birds, although recovery from non-sterile organs such as the caecum and duodenum remains elusive. Consequently, the route of transmission remains unconfirmed, although molecular detection by PCR of C. hepaticus DNA in the gastrointestinal tract and faeces of SLD infected birds is highly suggestive of a faecal-oral route.