VIGOSINE®: Management

of stresses in broilers
and laying hens

What is Stress?

Prevention and Management of Stresses

Informative Poster on the Measures to be taken

VIGOSINE® : Mode of Action and Results

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 Prevention and
management of
stresses in broilers
and laying hens
A variety of stressors exist in the rearing of broilers and
laying hens such as handling, transport, crowding and
immune challenge. These stressor factors last from a few
hours to several days or weeks.
I. Stress
Stress control is simultaneously integrated by the neural and I.1. Definition
I.2. What are the stress inducing
endocrine systems. This induces important changes in behavior, factors?
physiological parameters, especially hematological, enzymatic
II. Chronology of possible stresses
and hormonal. The stimulation of adrenal glands has a strong II.1. Chronology of possible stresses
impact on the liver, heart, kidneys and muscles. for broilers
II.2. Chronology of possible stresses
for laying hens
The changes listed above should be taken into account as they
III. Physiological mechanism
will be quantifiable parameters to measure the degree of
of stress
stress, to predict the impact on zootechnical performance and III.1. Alarm phase
to help implement treatments. III.2. Resistance phase : the bird tries
to adapt to its new living conditions
III.3. Decompensation phase
The first measure will be to eliminate the stress factors, as far III.4. The main stress indicators
III.4-a. Physiological indicators
as possible, and the second to rapidly distribute, dietary sup- III.4-b. Zootechnical indicators
plements into the drinking water, in order to restore appetite,
IV. Measures to be taken during
support the heart, liver and kidney functions and improve
stressful periods
immune defenses and prevent the risk of infection. IV.1. Stopping wasting and restarting
growth : restore apetite
IV.2. Preventing cardiac
and hepatic lesions
IV.3. Eliminating excess free fatty acids
IV.4. Supporting the kidney function
IV.5. Improving immune defenses
and preventing the risk of infection
IV.5-a. Vitamin supplementations
IV.5-b. Antimicrobial treatments

3
I. Stress
I.1. Definition
I.2. What are the stress inducing
Stress is "the result of excessive demands on the physiological
and behavioural capacities of the bird to adapt’’ (Dantzer). factors ?
Each bird is adapted to a given life environment (temperature, The bird's comfort zone is defined by a state of equilibrium of
feed, housing, physiological status...) within which the organism six factors: breeder, feeding, building, bird, microbism and
can fully express its genetic potential : this is the comfort zone. flock management (see Figure 1). This equilibrium
continuously evolves all along the bird's life (feeding and phy-
Sudden changes in one or several parameters of this environ- siological stage for example). Only a sudden change in one of
ment cause the bird to exhibit an adaptation reaction called these factors results in an imbalance: a stress.
stress. These environmental changes bring the bird out of the
comfort zone, then it can no longer compensate for these
changes and enters a stress period.

Fig. 1 - The six factors of equilibrium

The various factors inducing a stress reaction can be grouped under the generic name of aggression factors:

Breeder:
- Know-how (during handling,
Feed:
e. g. vaccination),
- Amino acid, energy, vitamin,
- Sense of observation.
mineral deficiencies,...
Flock
- Imbalances (Ca/P, lipids...),
management:
- Insufficient watering.
- All in-all out flock
breeding,
- Elaboration of the
group pecking
order (competition
at feeding trough,

-
fights...),
Light program,
Comfort
-
-
Type of containment,
Litter. zone Building:
Microbism: - Sudden temperature
- Hygiene (cleaning, changes (day/night,...),
disinfection, ventilation - Excessive population density,
space ...), - Insufficient ventilation
- Sanitary status: pathology or healthy carriage (accumulation of noxious
resulting in immunodepression or paving gases : ammonia, carbon
the way for other bacteria dioxide...),
(Gumboro, Mycoplasma, Colibacillus...), - Equipment.
- Parasitism, Bird:
- Handling: injections, debeaking (wounds...), - Various physiological changes:
loading, de-packing, relocation,... - Hatching,
- Live vaccines, - Starter,
- Debeaking, - Puberty (laying maturity),
- Nervosity, - Moulting...

4
II. Chronology of
possible stresses
All these factors have very few consequences when they are indi-
vidually active. However, this is seldom the case. Indeed, they are
II.2. Chronology of possible
most of the time combined. Throughout the bird's life, there are stresses for laying hens
critical phases liable to result in significant stress situations.

This rapidly results in the appearance of pathologies and/or stron-
gly impairs the technical and economic performance of the flock.
The following tables give examples of possible stresses in
broilers and layers.
Similar stresses are observed in layers during the first sta-
ges. Then, layers entered a very critical period from the start
of laying until the peak of lay which will impact the overall
laying performance (see Figure 3).
Fig. 3 - Chronology of possible stresses for laying hens

Critical periods Stress-promoting factors

II.1. Chronology of possible - Fatigue of the chick

- Microbism (ambient or latent carriage)
stresses for broilers Hatching immaturity of the main physiological
functions
For broilers, hatching, the starter period
- Immature physiology transport
and growth are the critical phases (see
- Microbism (miscellaneous origins)
Figure 2). The starter period is a difficult
Starter breeding conditions
physiological stage for the chick (imma-
(temperature, watering)
turity of its major functions), birds with
- Handling
different immune statuses are mixed,
- Vaccination with a live vaccine
there is competition at the feeding trough
(liable to result in feed deficiencies in the
weakest birds), increased microbism (due to the - Increase in density
concentration of birds), sometimes combined with incomplete - Pecking order microbism
cleaning-disinfecting-ventilation space of the premises. Growth - Temperature, ventilation handling
(vaccinations and other injections)
Fig. 2 - Critical periods for broilers - Vaccination with a live vaccine
Critical periods Stress-promoting factors
- Physiological disturbances
- Fatigue of the chick Laying - Psychological disturbances
Hatching - Microbism (ambient or latent carriage) maturity (lighting program, change of building,
immaturity of the main physiological of feeding...)
functions
- Flock management
- Immature physiology transport (containment mode...)
- Microbism (miscellaneous origins) Laying period - Vaccinations
Starter breeding conditions - Density of population
(temperature, watering)
- Handling Moulting - Physiological disturbances
- Vaccination with a live vaccine

- Increase in density
- Microbism temperature, ventilation
Growth
- Feed transitions
- Vaccination with a live vaccine

5
III. Physiological
mechanism of stress
The adaptation reaction of the organism to an aggression can be divided into 3 phases (see Figure 4):
Fig. 4 - Physiopathology of stress (Ruckebusche, 1981, Selye, 1985)
Stress phase Organ involved Consequences Clinical
- Orthosympathetic - Wakefulness state
A nervous system
Alarm phase - Hormone: adrenaline - Tachycardia, Tachypnea, - Nervosity
G Mydriasis Piloerection - Breathlessness
- Mobilization of Glucose and - Dishevelled
G
free fatty acids feathers
R
- Hormone: aldosterone - Sodium retention - Dishevelled feathers
E - Potassium excretion - Wet litter
S
Resistance phase - Hormone : ACTH - Hypocholesterolemia - Symptom(s) of the
S - Lymphoid atrophy accompanying
I - Lymphopenia pathology(ies)

O - Hormone: Cortisol - Immunodepression

N Decompensation - Exhaustion - Death - Mortality
phase of the organism

Recovery phase - Recovery of the organism - Gradual clinical recovery - Delayed growth

III.1. Alarm phase III.2. Resistance phase: the bird

The bird that undergoes a shock reacts through the periphe-
ral (orthosympathetic) nervous system. It is then in a wake-
fulness state.
This reaction is reinforced by the secretion of adrenaline (the
hormone of the adrenal gland) the effect of which consists in
increasing the general metabolism.
This effect results in:
- Increased cardiac rate (tachycardia),
- Lung hyperventilation (tachypnea),
- Dilatation of the pupilla (mydriasis),
- Dishevelled feathers (piloerection),
- Increased consumption of dietary energy
(carbonhydrates, lipids)
In the wild state, this results in the bird fleeing away, which
cannot happen in intensive breeding.
tries to adapt to its
new living conditions
For that purpose, it mobilizes numerous hormones:
The ACTH which produces:
• Hypocholesterolemia and increased lipid accumulation in the liver,
• Atrophy of the lymphoid organs such as the thymus and
Fabricius' bursa which play a part in the defense of the organism,
• Release of cortisol causing (see Figure 5):
- muscle wastage due to protein catabolism,
- retarded development of heart that can aggravate
hypoxaemia and ascites,
- hyperglycemia due to glycogenolysis/gluconeogenesis,
- enhanced secretion of insulin leading to a redistribution
of energy towards fat abdominal deposit,
- hyperuricemia,
- suppressed immune / inflammatory responses resulting
in immunodepression

6
 Fig. 5.a - Effect of cortisol on breast development from
% 28 d to slaughter age (Lin, 2006)
18 -28%
16
-16%
14
12 III.3. Decompensation phase
10
8
If aggression persists, it leads to the exhaustion of the organism:
6
• mobilization, use and exhaustion of energy reserves,
4
• fatigue of the various vital organs such as the heart
2
0
and kidneys,
21 28 35 42 • wear of the main functions such as immune defenses.
Age (days)
Breast weight (%) Control Breast weight (%) CORT The bird is thus weakened and extremely sensitive to the patholo-
gical and/or opportunistic bacteria present in its
Fig. 5.b - Effect of cortisol on abdominal fat deposit from environment. (Figure 6). This results in the bird's death (exhaus-
% 28 d to slaughter age (Lin, 2006)
tion and/or pathology) or the economic non-value of its production.
3
+46% If the aggression stops before or at the very beginning of this
2,5 phase, the bird may entirely recover and be cured, but its
2 +50% growth will be delayed.
1,5
Fig. 6 - Suppressive effect of ACTH, cortisol or cold stress
1 treatment on the non-specific immunity against E. coli infection
0,5 O1:K1 (p<0,05) (Matsumoto, 2000).
Viable count of
0 6 E. coli in spleen :
21 28 35 42 Log 10 (CFU/g)
Age (days)
5
Abdominal fat (%) Control Abdominal fat (%) CORT d
4
c
The defense/aggressor equilibrium is then broken in favour of 3
the bacteria. This imbalance will occur all the more easily as b
2
the global metabolism of the organism is weakened (exhaus-
tion of energy reserves...). 1 a
0
Aldosterone, increased during this period, also results in uri-
nary discharge of potassium and sodium retention, 2 signifi- Control ACTH Cold stress Corticosterone
cant elements in cell metabolism. This phase is more or less a-d Means within column with different superscript differ
prolonged according to the aggression intensity. significantly (p<0,05)

7
III.4. The main stress indicators
There are not one but many indicators of stress. When ana-
lyzing stress, the choice of the indicator depends on the para-
meter being affected (well-being, profitability).
Usually, the consequences of the stress on health and pro-
III.4.b Zootechnical indicators
ductivity are studied, since deleterious repercussions on pro-
fitability are certain. In the breeding, the stress reaction produces a decrease in
zootechnical results (see Figure 8).
- Retarded growth,
- Increase in feed conversion,
- Drop in laying,
III.4.a Physiological indicators - Decreased egg quality,
- Increased mortality,
The main harmful consequences of stress are associated - Depreciation of carcasses,
with the undesirable physiological effects of glucocorticoids - Multiple-factor pathologies.
and catecholamines:
Fig. 8.a - Influence of chronic stress at 14 and 28 days of age
• Reduced appetite following the bird's adaptation to the on body weight gain (p< 0,0001) (Lin, 2004))
cause of the stress, g/d

• Reduced ability to digest; nutrients are not properly extrac- 100 -57%
ted from the feed, due to reduced digestive secretion causing 90
indigestion, increased feed conversion efficiencies,... 80
• Wasting due to hormonally-induced proteolysis, 70
-42%
• Excess of free fatty acids due to hormonally-induced lipoly- 60
sis and worsened by a carnitine deficiency, 50

• Reduction in the bird's defense mechanism due to depres- 40

sion of the lymphoid tissue. The ratio heterophil/lympocytes 30

(H/L) which is a valuable indicator is significantly increased 20

10
due to both significant heterophilia and lymphopenia. The bird
0
is less able to resist infections and parasites, leading to poor
14 28
health and high mortality (see Figure 7). Age (days)
Control Stress

Fig. 7 - Influence of bird density on the H/L ratio % Fig. 8.b - Influence of chronic stress at 14 and 28 days of age
(p<0,05) (Campo, 2005) g/g on feed intake (p< 0,05) (Lin, 2004))
0,9
69
0,8 -45%
68 -40%
0,7
67
0,6
66 +7%
% 0,5
65
0,4
64
0,3
63
0,2
62
0,1
61
0
60
14 Age (days) 28
Low density > 20 birds/m2
Control Stress

The economical consequences are then serious.

8
IV. Measures
to be taken during
stressful periods
Some stresses are directly related to the breeding conditions energy production increases
and so well known. Suitable prevention measures could be due to the catabolism of
implemented in order to help the birds manage at best those lipids and proteins.
stresses (starter period, start of laying, pathologies, feed This causes the break-
transitions, transport, …). down of muscle tissue
by proteolysis and
On the other hand, when the stress situation will be installed, thus wasting.
the objective will be to help the bird to recover as soon as The production of
possible its confort zone in order minimize the impact on the energy has to be
performances. re-establish by the
catabolism of lipids to
counter wasting , so
the amino acids are
used instead for growth.
IV.1. Stopping wasting and restarting
The first need for the bird is
growth: restore appetite to restore its appetite. The bird
needs to resume eating the normal
Under the effect of the stress, and more precisely due to the quantities required for its needs as quickly as
effect of the hormones released into the blood stream, possible.
The digestive functions should also be stimulated, particularly
by increasing the digestive secretions depressed by stress.
Then the full benefit of the feed can be absorbed by re-esta-
blishing normal digestion.
IV.2. Preventing cardiac
and hepatic lesions
A consequence of stress is an excess of fatty acids due to
intense lipolysis.
Excess free fatty acids consume carnitine.
Carnitine is a necessary element in the production of energy
from fatty acids: it acts as a transporter, and is essential in
allowing fatty acids to cross into the mitochondria, where
they can then be catabolized by β oxidation.
Carnitine is biosynthezised in the liver and kidneys.
The amount synthezised is sufficient to provide an adult's
minimum requirements under normal conditions, i.e. in the
absence of stress: carnitine is not considered as being an
essential nutriment.
When the free fatty acid/carnitine ratio is correct, beta-oxi-
dation within the mitochondria is optimal and the storage of
fatty acids functions optimally and toxic metabolites do not
build up.
10
An excess in free fatty acids causes an imbalance, with a defi-
ciency in carnitine and leads to fat overload.
This excess quantities of grease in the cell causes cell
damage that mainly occurs in the cells of the liver and heart.
Giving rapidly the required carnitine:
• Orients the energy-producing catabolism toward
the catabolism of fatty acids pathway, and not via the cata-
bolism of proteins,
• Allows a more rapid elimination of the excess free fatty
acids acting as a detoxifying role.
IV.3. Eliminating excess free
fatty acids
Both in relation to catabolism and the elimination of excess
free fatty acids, the body's emunctories, the liver and kidneys,
are required to work hard.
Supplements providing B vitamins (particularly biotin) and
vitamin E / selenium, sorbitol, magnesium sulphate, vegeta-
ble extracts acts in synergy with carnitine to stimulate the
hepatic function, intestinal transit, pancreatic secretions and
diuresis.
These ingredients complement perfectly carnitine's role, by
eliminating waste products and by stimulating the organism.
IV.4. Supporting the kidney function
Supporting the kidney function will promote elimination of
stress metabolites and excess potassium.
Betaine is one of the main osmolytes present in the avian kidney.
Dietary supplements with betaine-based formulations asso-
ciated with mild diuretics will be so recommended.

IV.5. Improving immune defenses
and preventing the risk
of infection
In case of a stress reaction, the organism produces some
substances (ACTH, cortisol) which induce as a side effect a
weakening of the defense system, the defense/aggressor
equilibrium is then broken in favour of the bacteria.
The pathological risks related to a
stress factor are always very
significant.
Among the pathologies that
appear with stress, respiratory
pathologies (CRD, Coryza, sinu-
sitis...) can be mentioned, but
other organs may also be affected
(e. g. joints).
11
IV.5.a Vitamin supplementations
As previously mentioned, the stress reaction strongly dis-
turbs the bird's metabolism, leading to an increase in energy
consumption. Now, this energy production consumes vita-
mins.Vitamins are substances which the bird cannot produce
by itself.
Vitamins A, B2, B6 and B12 are known to have an essential
role in maintaining the integrity of the organism at the
immune system level.
IV.5.b Antimicrobial treatments
Antimicrobial treatments will be implemented as required.
Regarding the bacteria, the most adequate molecule will be
chosen.
Certain macrolides are known to have a complementary
action : a direct fight against the bacteria through their
antibiotic action and an indirect fight through the stimulation
of the immune response. This allows the restoration of the
equilibrium disturbed by the stress.
12
14
 Application
of VIGOSINE in stress
®

management
n intensive poultry farming, stress can affect any bird whose
I metabolism is adapted to the demanding conditions of this
type of farming: bird handling is frequent, and behavioral pro-
blems caused by confinement and poor environmental quality
are common.

In stressful situations, there is a sudden requirement for

additional energy (for adaptation to stress), however, there is I. Action and VIGOSINE®
also a risk of steatosis since the fatty acids mobilized by the utilization program
I.1. Optimization of fatty acid
hormonal action (catecholamines, corticosteroids, glucagon) catabolism
I.2. Prevent of cardiac, hepatic
are not suitable for a correct production of energy. and kidney damage
I.3. Stimulation of feed intake
and digestive secretions
VIGOSINE® supplied via the drinking water is a convenient way I.4. Practical use of VIGOSINE®
during stressful periods
of assisting birds in meeting their energy requirements rapidly,
and hence to reduce any deleterious effects on zootechnical II. VIGOSINE® trial results
II.1. Results of VIGOSINE® in pullets
performance. - Protocol
- Results
- Conclusion
II.2. Results of VIGOSINE® on cardiac
mortality in broilers
- Protocol
- Results
- Conclusion

15
 I. Action and VIGOSINE ®

utilization program
The main harmful consequences of adaptation to stressful
situation are associated with the undesirable physiological
effects of glucocorticoids and catecholamines (Figure 1).
• reduced appetite following the bird's adaptation to the
cause of the stress,
• reduced ability to digest, nutrients are not properly extrac-
ted from the feed, due to reduced digestive secretion causing
indigestion, increased feed conversion efficiencies, ...
• wasting due to hormonally-induced proteolysis,
• an excess of free fatty acids due to hormonally-induced lipo-
lysis and worsened by a carnitine deficiency,
• a reduction in the bird's defense mechanism due to depression
of the lymphoid tissue. The bird is less able to resist infections
and parasites, leading to poor health and high mortality.
I.2. Prevent of cardiac, hepatic
and kidney damage
Excess free fatty acids cause cell damage due to excess quan-
tities of grease in the cell. This damage mainly occurs in the
cells of the liver, the kidney and the heart.
Weakening of the liver, which is clear in layers and fast-gro-
wing chickens, makes it essential to enhance liver function,
particularly in chronic stress situations.
VIGOSINE® improves elimination of excess fatty acids. In addi-
tion, salts and plant extracts have a detoxifying function that
promotes elimination of metabolic waste products.

Fig. 1 - Stressful situations: benefits of VIGOSINE®

I.3. Stimulation of feed intake
and digestive secretions
Reduce appetite
and ability to digest In stressful situations, there is a sudden requirement for addi-
Cell damage caused tional energy (for adaptation to stress). Paradoxically the stress
by excess fatty acids depresses the appetite and the digestive secretions. VIGOSINE®
Excess fatty acids
and carnitine STRESS by increasing appetite helps the bird to resume eating the nor-
deficiency mal quantities required for its needs more rapidly.
VIGOSINE® stimulates also the digestive functions: the full benefit
Hepatic overload, of the feed can be absorbed by restoring normal digestion.
Excess of metabolic cardiac and renal
waste products fatigue

Restores appetite
I.4. Practical use of VIGOSINE®
and stimulate digestive
functions
during stressful periods
Limits hepatic,
Enhances catabolism
cardiac and kidney VIGOSINE® is to be used regularly over short periods of time,
damage
of fatty acids particularly during difficult periods as far as feeding is concer-
and stops thinning VIGOSINE
ned (starter period, transitions and finisher period for the broi-
lers, start of laying and up until the laying peak for the layers).
Supports hepatic, Such use makes it possible to eliminate excess free fatty acids
Facilitates renal cardiac and kidney Distribute the product continuously using a dosing pump, or
excretion functions
pour sufficient product directly into the feed tank for half-a-
day's consumption.
Dosages are expressed as ml of VIGOSINE® per liter of drin-
king water.

I.1. Optimization Objective VIGOSINE®

- Recovering appetite 1-2 ml / liter for 1 to 3 days
of fatty acid catabolism - Utilising fatty acids during and after the stress
Excess free fatty acids, a consequence of stress, consume car- (lipolysis)
nitine and lead to a secondary deficiency. VIGOSINE® supplies
the bird rapidly with the required carnitine. It encourages the - Assisting filtering Broilers: 1 ml / liter for 2 to
catabolism to take the lipid pathway, stops wasting by preven- organs 4 days during feed transition
ting proteolysis, and enables growth to be rapidly resumed in - Preventing the Layers: 1-2 ml / liter for 2
order to attain correct zootechnical performance. infiltration of grease days every 3 to 4 weeks until
peak of lay.

16
II. VIGOSINE ®

trial results
Fig. 2 - Results of VIGOSINE® on consumption and weight
II.1. Results of VIGOSINE® of pullets after debeaking and vaccination
Average weight of

in pullets the laying hens (g)

Vaccination
Protocol Debeaking

A group of intended to be layers were vaccinated (fowl pox

and LTI) and debeaked when 10 weeks old. The farm had two
buildings, the birds in one were given aspirin at a dose of
0,25g/l for 3 days after the two operations (control popula-
tion: 33 462 pullets). The birds in the other house were given
aspirin at the same dose and VIGOSINE® at 2 ml/l for the 4 Age
days following two operations (treated population: 20 732 (weeks)

pullets).
Control VIGOSINE
Feed in take
Results (g/hen/day)

Immediately after vaccination and debeaking, a reduction Vaccination

Debeaking
was observed in feed consumption for both groups, followed
by a reduction in live weight during the following week.
The recovery rates for the two groups were however different
(Figure 2).

The control group recovered normal consumption levels 4

weeks after the operation; live weight was recovered at a Age
much larger stage. (weeks)

The two operations VIGOSINE® group recovered quasi normal Control VIGOSINE
consumption in the week after the operation, and caught up
with the standard growth level after 4 weeks. The average
live weight for the trial group was greater than the control by Conclusion
2% after 10 weeks, and 12% higher after 16 weeks.
This trial demonstrates that a moderate use of VIGOSINE®
(4 days at 2ml/liter) enables the pullets under vaccination and
debeaking stress to better withstand such stress and recover.

17
II.2. Results of VIGOSINE®
on cardiac mortality in broilers

Protocol
This trial assessed VIGOSINE® against a PLACEBO, each pro-
duct being used in a static-ventilation building housing
26,400 broilers (initial density: 22 broilers/m2).
As soon as the daily percentage of cardiac mortality of 0.1%
(verified by autopsy) of the population in either of the buil-
dings was reached, the products were randomly assigned to
the buildings and were given at the same time in each res-
pective building for 7 days at 2 ml/liter drinking water. Conclusion
Cardiac and overall mortality was then recorded each mor- While the sudden death rate naturally increased over period
ning at a set time, as well as performance for each period D16-D35, VIGOSINE® made it possible to reduce these los-
(growth, feed conversion). ses although the group was heavier than the control group at
the end of the rearing period. These results show that VIGO-
SINE® reduces the risk for cardiac mortality while optimizing
Results growth.
Cardiac mortality reached 0.13% at 16 days in one of the The effect on the MDG was observed during the period when
buildings (B1), while it was 0.10% in the other (B2). VIGOSINE® was given; these results suggest that it is prefe-
Products were added to the drinking water between 16 and rable to use VIGOSINE® over short periods of time (1 day at
23 days of age. 1 ml/liter), on a frequent basis (once to twice a week), rather
In both groups, cardiac mortality increased: +0.5% in the than using it continuously.
VIGOSINE® group (B1) versus +0.8% in the PLACEBO group
(B2) (Figure 3). Fig. 4 - Effects of VIGOSINE® on growth

While the VIGOSINE® group had a lower weight prior to sup- 1.6
plementation (-5.5% at D16), its showed a significantly 1.4
higher live body weight at the end of supplementation (+7.1% 1.2
at D23), and this difference was still partly found at slaugh- 1
ter (+4.1% at D35) (Figure 4). 0.8
0.6
Fig. 3 - Effects of VIGOSINE® on cardiac mortality 0.4
0.2
0.80 0
D16 D23 D35
0.70
Placebo VIGOSINE

0.60

0.50

0.40
D1 - D15 D16 - D23 D23 - D35

Placebo VIGOSINE

18
References
• ARSLAN. C,
L-carnitine and its use as a feed additive
in Poultry feeding a review
Revue de médecine vétérinaire, 2006,
156, 3, 134-142
• ASLAM and al.
Effect of stress following vaccination
against Newcastle Disease broilers.
JAPS, 2005, Vol. 15, n°34, p 56-59
• AVANZO and al.
Effect of vitamin E and selenium on
resistance to oxidative stress in chicken
superficial pectoralis muscle.
Comparative biochemestry and physio-
logy., 2001, vol. 129,n°2, p.163-73
• BIEBER L.L.
Carnitine
Annual Review of Biochemistry, 1988,
57, 261-283.
• CAMPO and al.
Effect of intermingling chicks and bird
density on fear and stress responses in
chickens. Archiv fuer Geluegelkunde,
2005, Vol 69,n°5,p 199-205
• COLLECTIF
Lipid metabolism.
In: Avian physiology, P.D. Sturkie Editor
1986, 345-358.
• KHALED-N-F and al.
Influence of dietary L-carnitine
supplementation on performance,
serum traits, carcass composition and
stress responses of broilers fed low-or
high-fat diets
Vetrinary Mediacl journal GIZA, 2005,
vol. 53; n°2, p 577-590
• GALLAGER-JP and al.
CRF is the “egg and Chicken”, whereas
ACTH and corticosteroids are only
“chickens” in response to stress.
Psychoneuroendocrinology, 2006,
Vol/Iss/pg 31/1 (142-143)
• GOA K.L., BRODGEN R.N.
L-Carnitine
Drugs, 1987, 34: 1-24
• GOSH-ASHOK and al.
Stress and avian adrenal function
Biomedical research, 2002,
Vol 13, n°2-3, p 60-74
• HARPEY J.P.
Le système carnitine
Cahiers de Nutrition and de Diététic,
1993, 28: 5, 274-283.
• JACOB C., BELLEVILLE F.
L-Carnitine: métabolisme,
fonctions et intérêt en pathologie.
Pathologie biologie, 1992,
40: 9, 910-919.
• LARBIER M., LECLERCQ B.
Métabolisme énergétic.
In: nutrition et alimentation des volailles,
Editions INRA 1992, p.63-90.
• LEBOUCHER R.
Moins de mortalité "cardiaque",
un GMQ amélioré...
Un apport nutritionnel au banc d’essai.
Filières avicoles, n°566 mai 1995,
69-70.
• LIN and al.
Oxidative stress induced by
corticosterone administration in broilers
chickens (Gallus gallus domesticus) :
1 Short-term effect.
Comparative Biochemistry and physio-
logy. 2004, Vol. 139, n°4, P. 745-751.
• LIN and al.
Oxidative stress induced by
corticosterone administration in broilers
chickens (Gallus gallus domesticus) :
2 Chronic exposure
Comparative Biochemistry and physio-
logy. 2004, Vol. 139, n°4, P. 737-744.
• MATSUMOTO and al.,
Induction of short term, non-specific
immunity against E. coli infection in
chickens is suppressed by cold stress
or corticosterone treatment.
Avian Pathology, 2000, Vol 29,
n03, p 227-232
19
• MOGENET L., VALANCONY H.
Un apport nutritionnel testé dans l'eau
de boisson: un “plus” contre les coups
de chaleur.
Filières avicoles, n°579 juillet-août
1996, 57-59.
• MOGENET L., VALANCONY H.
El VIGOSINE y los golpes de calor
Selecciones Avicolas, Vol. 38, n°8,
agosto 1996, 496-502.
• POST-J and al.
Automaed blood cell count:
a sensitive and reliable method to study
corticosterone-related stress in broilers;
Poultry science, 2003, vol. 82, n°4,
p591-595
• REBOUCHE C.J.
Carnitine metabolism
and functions in humans
Annual Review of Biochemistry, 1986,
6, 41-66.
• RETTENBACHER-S and al.,
Measurement of corticosterone
metabolites in chicken droppings.
British poultry Science, 2004,
Vol 45, n°5, P 704-711.
• RUCKEBUSCHE Y.
"physiologie pharmacologie
thérapeutique animales"
Maloine, 2° édition, 1981.
• SELYE H.
in dossier Interne SSNA, 1985.
• TANIGUCHI and al.,
A high doe of vitamin E inhibits adrenal
corticosterone synthesis in chicken
treated with ACTH, Journal of nutritional
science and Vitaminology, 2001,
Vol. 47, n°1, p. 40-6
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