Intensive broiler chicken production systems and the infectivity of - PowerPoint PPT Presentation

Intensive broiler chicken production systems and the infectivity of Campylobacter Tom Humphrey t.j.humphrey@swansea.ac.uk

By 2030: Agricultural production More people means less cultivated land per person for food Animal production will become more intensive Where does animal welfare fit in? 2030 – 8.3 bn people 2030?

Campylobacter • Important to study in its own right • Good model for study of environmental and management influences in animal production • Estimated 750000 cases annually in UK 80000 • ~ 3 cases every 2 minutes Confirmed cases in England and Wales 70000 • 1% of EU population 60000 • Elderly people more at risk 50000 • Main vehicle is chicken 40000 30000 20000 1 reported case = 10 in the community 10000 0 89 90 91 92 93 94 95 96 97 98 99 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Year

We tend to eat chicken produced intensively

Chickens have been taken a long way • From luxury food to a regular item in 40 years • Achieved by industrialisation of production • Selective breeding for fast growth • Modern broiler reaches 2.2Kg in ~35 days • Production needs to quadruple • Separation from animal health and welfare • Major implications for public health

Campylobacter and chicken: two health threats • High level surface contamination (10 9 ): A cross-contamination risk • Contamination of liver and muscle tissues: Heightened risk from under-cooking (20% muscle +) • ~80% of cases chicken-related • Many chicken liver paté outbreaks • Eating chicken out, a major risk factor

Infection of edible tissues (extra-intestinal spread) is more likely: • In birds that are suffering acute or chronic poor welfare • In birds co-infected with E. coli • If the gut is inflamed: poor diet and/or endemic disease • If gut microbiota has been disturbed by antibiotic treatment and/or stress • Naturally occurring LAB inhibit C. jejuni • In acutely stressed birds, LAB fell by 90% • LAB are important in control

Improving chicken welfare will improve public health • Current campaigns focus on animal welfare alone • These may not be powerful enough to bring about change • Consideration should also be given to public health impacts of poor welfare

Hypothetical dynamics of chicken infection with Campylobacter • Extensive production : frequent challenge with high numbers of undamaged Campylobacter • No effective barriers to infection • Housed production : infrequent challenge with a few sub- lethally damaged Campylobacter • More difficult for pathogen to establish • Primary infection in birds, where disease resistance compromised by poor health and/or welfare • The more compromised birds, the more likely the flock will be colonised • Whether it’s an elderly man with cancer or a compromised chicken, C. jejuni benefits from a “damaged gut”

Impacts of acute stress

In vivo behaviour of C. jejuni in chickens strongly linked to welfare of the host • Chickens experience acute and chronic stress • Responses to endemic disease and/or environment important • Change pathogen behaviour • Create invasive phenotypes of Campylobacter • A need to better understand effects of production environments • End of life common to all systems

Noradrenaline increases C. jejuni growth in low iron environments 1.0 +NA 0.8 OD at 600nm 0.6 NA 0.4 0.2 -NA 0.0 0 6 12 18 24 30 36 42 48 Higher levels seen in birds post-transport NA acts as an iron-capture mechanism Iron-rich Campylobacter are more virulent

C. jejuni pre-treated with noradrenaline more invasive in chickens 70 % positive 60 50 40 + NA 30 Cont 20 10 0 Liver Caeca This models spread from “stressed” birds Increase in activity of iron-regulated virulence genes

Is Campylobacter jejuni now having a direct impact on broiler welfare and performance?

Campylobacter and chickens • An opportunistic pathogen in some broiler types • Immune responses designed to keep it in the gut, not to clear it • In vivo behaviour is influenced by state of the chicken host • Results can differ between ‘farm’ and ‘laboratory’ studies • Chickens differ in innate responses: Campylobacter differ in ‘virulence’ Liver T cells of infected birds proliferate on stimulation by C. jejuni Fig 2: Chickens ’ immune responses to campylobacter differ from those to other “ commensals ” 1200 1200 IgY titre 1000 1000 800 800 600 600 Camp mp LAB 400 400 200 200 0 7 28 28 Days

Research that started the work on broiler systems, bird health and Campylobacter Published in the 2 nd ACMSF report 2002. Work done with Lloyd Maunder Ltd in late 1990s. Over 7 flock cycles Farm A had 1.4% positive birds and Farm B had 97%. This led to funding from FSA

Outputs from work with Lloyd Maunder Ltd from the FSA project • When tested pre- thinning, ‘slow birds’ had lower Campylobacter than ‘fast’ ones. • Levels of condemnation for ‘APEC’ infection and levels of hock marks lower in ‘slow’ birds • Highly significant link between APEC, poor gut health and Campylobacter % birds Campylobacter -positive 80 70 60 STD 50 FF 40 30 20 10 0 1 2 3 4 5 6 7 8 9 • Similar data on differences in leg health seen in matched studies in: - UK (Pagazaurtundua and Warriss 2006) - The Netherlands (de Jong et al. 2012)

Other work on broiler health, welfare and Campylobacter (2) Colles et al . (2008): “Campylobacter diversity was significantly affected by average flock growth rate and incidence of worse hock burn so that diversity increased” Russell SM (2003): symptoms consistent with APEC increased Campylobacter levels on carcasses Subler et al (2006): IBDV-Induced immunosuppression exacerbates C. jejuni shedding in chickens Lawes et al (2012): Campylobacter positivity was associated with higher recent mortality level in the flock Powell et al (2012): Increased mortality at 14 days was a risk factor for carcasses highly contaminated with Campylobacter

Broiler genotype, leg health and Campylobacter • Past work found – High levels of hock marks and pododermatitis were risk factors for Campylobacter infection in commercial flocks, pre-thinning We assumed that hock marks/pododermatitis preceded Campylobacter and that the bacteria better colonised a ‘damaged’ gut, however.................................

Infection with C. jejuni M1 can be associated with leg health problems Number of cases of hock marks and pododermatitis observed at the final timepoint (16 dpi) from both the fast (n=49) and slow growing (n=50) breeds of birds either given C. jejuni (+) or a placebo control (-). Asterisk indicates a significant difference P=0.05. Williams et al 2013

Innate responses to C. jejuni M1 differ between broiler types 2 4 6 8 10 12 3 4 10 Regulation 8 Predcited levels CXCLI2 (blue) il10 (red) 6 4 2 0 1 2 10 Inflammation 8 6 4 2 0 2 4 6 8 10 12 Time Immunological response of four broiler types as a function of time In birds that get diarrhoea there is a marked and prolonged inflammatory response

In some broilers, C. jejuni M1 causes damage to gut epithelia Profound diarrhoea Little diarrhoea

Campylobacter infection and broiler performance Sparks et al. 2013) Campylobacter -negative commercial flocks had better FCR (1.666 vs 1.690) (Data are robust and no other parameter had an effect) Awad et al Innate Immunity (2014) • Infection affected performance • At 7 dpi BM was 510 g in infected birds and 620 g in controls (p<0.1) • FCR for infected birds was 1.81 and was 1.41 for controls • No diarrhoea was seen . C. jejuni NCTC 12744 used