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Novel insights in the pathogenesis and control of necrotic enteritis/dysbacteriosis in broilers
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Novel insights in the pathogenesis and control of necrotic enteritis/dysbacteriosis in broilers
Prof. Dr. F. Van ImmerseelGhent University
Faculty of Veterinary MedicineDept. Pathology, Bacteriology and Avian Diseases
Gut health: what are important factors?Nutrition
• Optimal nutritional quality, free of pathogens and toxins
• Feed should be broken down by digestive and non-digestive enzymes, to exclude presence of residual nutrients in gastro-intestinal tract
• Viscosity should be low
• Nutrition and feed additives can influence gut microbiota composition
• Using nutrition changes we can predispose to NE/dysbacteriosis
Gut health: what are important factors?Gut microbiota composition
• Both quantity and quality are important, depending on gastro-intestinal segment
• Stability and diversity of microbiota is important !• Richness (number of species) and eveness (relative abundance
of species) are important !
ileum LactobacillusClostridiumEnterococcusStreptococcusWeisellaStaphylococcusCampylobacterEubacteriumFusobacteriumBacillusother
cecumClostridiumRuminococcusFusobacteriumEubacteriumLactobacillusBacteroidesBacillusEscherichiaEnterococcusother
Gut health: what are important factors?Gut wall morphology and integrity
• Villus structure should be optimal to preserve absorptive surface
• Epithelial cell proliferation and differentiation should be optimal
• Lesions/erosions should be avoided
• Epithelial cell damage or junction defects should be avoided
Gut health: what are important factors?Inflammation
• Immune cell infiltration should be kept as low as possible, without interfering with normal repsonses
Factors affecting gut health
Optimal gut health
Balanced intestinal microflora
Optimal animal performance
Nutrition and management
Gut wall morphology, integrity and inflammation
Necrotic enteritisNecrotic enteritis
• Enteric disease in broilers
• Age-specific onset, 2-4 weeks post hatch
• Clostridium perfringens
Worldwide estimated losses due to necroticenteritis:
2 billion $ annually
Ban on antibiotic growth promoters (AGP) in EU (01-01-2006)
Clostridial Enteritis – The Profit Killer
Typical growth retardation caused by clostridial enteritis at the third week of life
Source: Sluis W Van Der, World Poultry 2000
In practice, necrotic enteritis in chicken occurs mostly between 15-35 days of life, with a peak at 20-25 days of life
Only after 10-12 days of life an anaerobic microflora is established in the gut
010203040506070
7 14 21 28 35 42days
daily
wei
ght g
ain
(gra
m)
Control broiler Broiler with Clostridium infection
Onset of necrotic enteritisOnset of necrotic enteritis
+
not necessarily disease!!
PREDISPOSING FACTORS !!
Predisposing factorsPredisposing factors
• Coccidiosis
• Feed
• Others
- Hygiene / shed management
- Stocking density
- Immunosuppression
d16 d17 d18 d19 d20 d21 d22 d23 d24
Gumboro vaccine x
Feed + fishmeal (30%) x x x x x x x x
10-fold dose of Paracox-5 x
Oral inoculation with
C. perfringens strain 56x x x x
Autopsy x x x
Experimental in vivo model for sub-clinical NEExperimental in vivo model for sub-clinical NE
40-70% of infected birds present necrotic lesions(Gholamiandehkordi et al., 2007)
Experimental in vivo model for sub-clinical NEExperimental in vivo model for sub-clinical NE
Necrotic lesions
Isolate number Health status of
the flock of origin
Toxinotype Alfa toxin
production
7 Healthy A Low
8 Healthy A Intermediate
17 Healthy A High
48 Necrotic enteritis A High
56 Necrotic enteritis A Intermediate
61 Necrotic enteritis A Low
Testing different C. perfringens strainsTesting different C. perfringens strains
0
10
20
30
40
50
60
negative control
paracox 7 8 17 48 56 61
per
cen
tage
of a
nim
als
wit
h le
sio
ns
group
Testing different C. perfringens strainsTesting different C. perfringens strains
Results
• Only isolates from NE cases induce necrotic lesions
• Ability to induce disease is independent of ability to produce alpha toxin
Strain Birds with lesions (%) netB
7 0 -
8 0 -
17 0 -
48 11.11 +
56 48.15 +
61 55.56 +
Necrotic enteritis specific toxinNecrotic enteritis specific toxin
Different C. perfringens toxins, different activities, different host range?
HOST-SPECIFIC TOXINS ???
εβ
ε ι
βEnter
otoxin
netB
α
α
α
NetB toxin
NetB mutant is unable to cause necrotic lesions !
Keyburn et al. (2008).
PLOS Pathog. 4(e26).
Single strain dominanceSingle strain dominance
• Isolates from a NE outbreak are highly clonal in the flock
• C. perfringens strains isolated from broilers are genetically heterogeneous
‘Spot-the lawn’ test‘Spot-the lawn’ test
growthinhibition
no growthinhibition
Results
• Virulent strains are more capable of inhibiting other C. perfringens strains
• Strains that produce peptides that inhibit other C. perfringens strains
overgrow the others
Granulocyte rim
Bacteria
Necrotictissue
What can we do?
٢٢
•Kill the bacteria
•Prevent predisposing factors•Coccidiosis (ionophores ...)• Stocking density, hygiene, ...• Optimize nutritional quality
•Vaccination? e.g. netB toxoid
•Feed additives?
Treatment with therapeutic antibiotics
٢٣
• Infection from day 17 until day 20
• Treatment in the drinking water from day 20 until day 24
Treatment with therapeutic antibiotics
٢٤
Percentage of birds with necrotic lesions over the 3 sampling days
(Lanckriet et al., 2010)
Protective effects of ionophore anticoccidials
٢٥
• Treatment in-feed from day 1
Protective effects of ionophore anticoccidials
٢٦
Percentage of birds with necrotic lesions over the 3 sampling days
(Lanckriet et al., 2010)
Protective effects of certain feed additivesProtective effects of certain feed additives
Treatment in-feed from day 1
Protective effects of certain feed additivesProtective effects of certain feed additives
Percentage of birds with necrotic lesions over the 3 sampling days
(Timbermont et al., 2010)
Vaccination ? (netB? Toxoid? Crude SN?)Vaccination ? (netB? Toxoid? Crude SN?)
Percentage of birds with necrotic lesions over the 3 sampling days
‘Trendy’ term pointing to a condition in which composition of microbiota is capable of decreasing performance due to poorly
described mechanisms, although pathogens are not necessarilypresent
Synonyms ???Feed passage syndromeMalabsorption syndromeWet litter syndrome…..
Dysbacteriosis
Macroscopic scoring
• Figure. Macroscopic dysbacteriosis score system parameters.
• A. Overall gut ballooning; • B. Content of the intestinal tract, 1. Mucoid, orange intestinal
content, 2. Foamy intestinal content; • C. Tonus of the intestinal tract, 1. Good tonus, 2. Lack of tonus; • D. Macroscopically visible thickness of the intestinal tract, 1.
Macroscopically thin intestinal tract, 2. Intestinal tract with normal thickness;
• E. Undigested particles in the colon (arrows); • F. Inflammation of the gut, 1. Inflammation, 2. No inflammation.
1000120014001600180020002200
1 2 3 4 5 6 7 8macroscopic dysbacteriosis score
villu
s le
ngth
(um
)
2 - 8
measured in µm in broilers at 21 days
0
50
100
150
200
250
1 2 3 4 5 6 7 8
macroscopic dysbacteriosis score
mus
clar
laye
r thi
ckne
ss (u
m) 2 - 8
0123456789
1 2 3 4 5 6 7 8macroscopic dysbacteriosis score
T-ce
ll in
filtra
tion
(% a
rea)
2 - 8
Dysbacteriosis: macrocopical signs in the gut
• Inflammation• Morphological damage (villi length decreases,
apoptosis, goblet cell proliferation)• Tunica muscularis thinning
Microbiota composition?
• Is it a dysbiosis of the gut microbiota???
Poly- or oligosaccharides
-oses
Lactate Acetate
Butyrate
Sulphate
H2S
Sulphate-reducingbacteria
Clostridium cluster XIVa
Clostridium cluster IV
How to control dysbacteriosis?
• Antibiotics• Feed composition• Products that are
– Antibacterial
– Anti-inflammatory
– Shift bacterial microbiota composition
Preventive products
• Acids• Essential oils
• Prebiotics: steering the microbiota composition to a favorable one (anti-inflammatory, less epithelialdamage)– Manno-oligosaccharides– Fructo-oligosaccharides – …
Thanks for your attention !