Group Title: Circular
Title: Hatchability problem analysis
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 Material Information
Title: Hatchability problem analysis
Series Title: Circular
Physical Description: 11 p. : ; 28 cm.
Language: English
Creator: Wilson, Henry R ( Henry Russell )
Publisher: University of Florida, Institute of Food and Agricultural Sciences, Florida Cooperative Extension Service
Place of Publication: Gainesville Fla
Publication Date: 1993
 Subjects
Subject: Eggs -- Incubation   ( lcsh )
Incubators   ( lcsh )
Chickens -- Hatcheries   ( lcsh )
Chickens -- Diseases   ( lcsh )
Genre: government publication (state, provincial, terriorial, dependent)   ( marcgt )
bibliography   ( marcgt )
non-fiction   ( marcgt )
 Notes
Bibliography: Includes bibliographical references (p. 10-11).
Statement of Responsibility: H.R. Wilson.
General Note: Title from caption.
 Record Information
Bibliographic ID: UF00008570
Volume ID: VID00001
Source Institution: University of Florida
Holding Location: University of Florida
Rights Management: All rights reserved by the source institution and holding location.
Resource Identifier: ltqf - AAA6834
ltuf - AJU3485
oclc - 29506700
alephbibnum - 001868955

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Circular 1112
UNIVERSITY OFircular 1112

v' FLORIDA


Hatchability problem analysis

H. R. Wilson*

University of Florida / Institute of Food and Agricultural Sciences / Florida Cooperative Extension Service / John T. Woeste, Dean


Introduction
When a problem occurs in hatchability, usually
it can be categorized as a hatchery, egg handling,
or breeder flock problem. If the problem has origi-
nated within the breeder flock, it is probable that
it happened at least 4 weeks earlier, assuming 3
weeks of incubation and 1 week of egg storage.
This delay in identifying a problem is costly and
may even make it impossible to determine the
cause if the effect is of short duration. It is neces-
sary to identify the problem as early as possible,
using candling at 1 week of incubation and con-
stantly monitoring unhatched eggs, to minimize
the delay in taking corrective measures. Analysis
of hatch debris does not yield definitive diagnoses;
however, it is a useful tool for determining the
most likely areas for further examination.

It is of utmost importance for hatchery, egg han-
dling, and breeder farm personnel to work together
as a team to produce top quality chicks and to iden-
tify problems when they occur. Very accurate and
complete records of the breeder flock (including
egg production, mortality, morbidity, egg weight,
shell quality, hatchability, feed consumption, and
antibody titers) and the egg history from the nest
through the hatchery are essential in providing
clues to most hatchability problems. Personnel
should be trained in recognizing problems, iden-
tifying causes, and implementing appropriate
corrective measures.

The objective of the following outline is to
suggest possible causes, and corrective measures
when appropriate, for some of the signs of trouble
observed when decreased hatchability occurs.


General comments
The magnitude of the effects of deviations from
recommended incubation conditions (temperature,

*Poultry Science Department, University of Florida,
Gainesville, Florida 32611.


humidity, turning frequency, ventilation, and
egg orientation) is a function of the severity of the
deviation, the length of time of the deviation, and
the age of the embryo at the time of the deviation.
The manifestation of abnormalities and the embry-
onic age at which mortality peaks occur due to
nutritional factors usually depend upon the sever-
ity of the nutrient deficiency, how long the defi-
ciency has existed, or how long an adequate diet
has been fed to the breeders following a deficiency.
Therefore, depletion rate, repletion rate, egg depo-
sition efficiency, interference from inhibitors, and
yolk formation time are factors that contribute to
the effects manifested in embryonic abnormalities
and mortality.


Troubleshooting:
General problems

1. Sign: Eggs candle clear; broken out eggs
show small white-dot germinal disc;
no blood. Infertile.

Causes:
a. Immature males. Males may need to be
photostimulated 2 weeks earlier than
females.
b. Males with abnormal sperm; females
with abnormal egg (germinal disc). This
occurs most often in very young or very
old breeders.
c. Too few males, resulting in infrequent mat-
ing; too many males, resulting in fighting or
interference. Ratios of 1:12 to 1:15 for light
breeds and 1:10 to 1:12 for heavy breeds are
suggested.
d. Extreme weather conditions.
e. Old breeders. Spiking with young males
may help if the problem is with the male.
f. Breeder flock disease. This is often indicated
by rough, misshaped, or thin-shelled eggs.








g. Excess body weight, especially in broiler
breeder males (>4,800 g, 10.6 lb).
h. Nutritional deficiencies or excesses; severe
feed restriction.
i. Feet and leg problems, especially in males
of heavy breeds.
j. Certain drugs, pesticides, chemicals, toxins,
or mycotoxins.
k. Parasites, such as mites.
1. Inadequate floor space.
m. Decreased mating frequency, or no mating,
is commonly seen in many of the conditions
listed above; this may often be the direct
cause of infertility.
n. Inadequate lighting (intensity or daylength).
o. Improper artificial insemination procedures
(if artificial insemination is used).

2. Sign: Eggs candle clear; broken out eggs
show enlarged germinal disc; no blood.
Fertile. Some are termed blastodermm
without embryo."

Causes:
a. Eggs stored too long. They should be stored
<7 days.
b. Eggs held under poor conditions, tempera-
ture too high or too low. Fluctuating tem-
peratures. Temperature should be 60 to
65F (15.60 to 18.30C).
c. Fumigation improper too severe or
done between 12 and 96 h of incubation.
Incorrectly spraying or foaming eggs with
disinfectant.
d. Eggs damaged during handling and trans-
port by jarring, temperature shock (tempera-
ture increased or decreased too rapidly), etc.
e. Eggshell sealed respiration inhibited.
f. High temperature in early incubation.
g. Very young or very old breeders.
h. Heredity, inbreeding, chromosome abnor-
malities, or parthenogenesis.
i. Breeder flock diseases.
j. Failure of a basic organ system to develop
normally.
k. Egg wash temperature too high.
1. Egg-borne infections (e.g., salmonella).
m. Drugs, toxins, pesticides, etc.
n. Infrequent or incomplete egg collection.
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F- 3 <

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3. Sign: Eggs candle clear; broken out eggs
show blood ring or small embryo that died
before 3 days of incubation; no dark eye
visible.

Causes:
a. Eggs stored too long or under improper
temperature.
b. Fumigation improper too severe or done
between 12 and 96 h of incubation.
c. High temperature in early incubation.
d. Low temperature in early incubation.
e. Eggs damaged during transport by jarring,
etc.
f. Breeder flock diseases.
g. Old breeders.
h. Embryological development accidents.
i. Inbreeding, chromosome abnormalities.
j. Severe nutritional deficiencies, e.g., biotin,
vitamin A, copper, vitamin E, boron, or
pantothenic acid.
k. Frequently associated with a high incidence
of infertility.
1. Drugs, toxins, or pesticides.
m. Contamination.
n. Embryos less developed at oviposition,
i.e., pre-endoderm or very early endoderm
formation.

4. Sign: Dead embryos; 3 to 6 days of incuba-
tion; yolk sac circulatory system present,
embryo on left side, no egg tooth.

Causes:
a. See causes 3.a-n.
b. Lack of ventilation, or sealed shells, carbon
dioxide >1%.
c. Improper turning 6/h; improper
turning angle.
d. Vitamin deficiencies vitamin E, riboflavin,
biotin, pantothenic acid, or linoleic acid.

5. Sign: Dead embryos; 7 to 17 days of
incubation; each embryo has egg tooth,
toenails, feather follicles (8 days), feathers
(11 days).

Causes:
a. Improper incubator temperature, humidity,
turning, ventilation. Low humidity increases
abnormalities of aortic arches (13 days).








b. Contamination.
c. Nutritional deficiencies riboflavin,
vitamin B12, biotin, niacin, pyridoxine,
pantothenic acid, phosphorus, boron, or
linoleic acid.
d. Lethal genes (>30 have been described).

6. Sign: Dead embryos; >18 days of
incubation.

Causes:
a. Improper incubator temperature, humidity,
turning, ventilation.
b. Improper hatcher temperature, humidity,
ventilation.
c. Contamination, especially from molds
(aspergillis, etc.).
d. Fumigation too severe or too prolonged.
e. Eggs chilled in transfer, or transferred too
late.
f. Broken shell pre-set, during incubation,
or at transfer.
g. Nutritional deficiencies vitamin D,
vitamin A, folic acid, or pantothenic acid,
riboflavin, vitamin E, selenium, vitamin K,
biotin, thiamin, vitamin B12, calcium,
phosphorus, manganese, or linoleic acid.
h. Embryonic malposition; embryo fails to move
into proper hatching position (see #21).
i. Embryological development accident.
Failure to change to lung respiration and all
intra-embryonic circulation, and/or to retract
the intestinal loops and yolk sac. These and
other changes are critical at this time.
j. Heredity lethal genes, chromosome
abnormalities.
k. Twinning.
1. Hatcher opened too much during pipping
and hatching.
m. Poor shell quality.
n. Breeder diseases.


Troubleshooting:
Specific problems

7. Sign: Not pipped. Full-term embryo, large
yolk sac; yolk sac may not be fully enclosed
by abdominal wall, may have residual
albumen.


Causes:
a. Inadequate turning, resulting in decreased
embryonic membrane development and
nutrient absorption.
b. Humidity too high during incubation or
after transfer.
c. Incubator temperature too low.
d. Hatcher temperature too high.
e. Eggs chilled (e.g., at transfer).
f. Nutritional deficiencies.
g. Heredity.
h. Embryological development accident.
i. Breeder diseases.
j. Inadequate ventilation.
k. Prolonged egg storage.

8. Sign: Pipped. Full-term embryo, dead in
shell.

Causes:
a. Low humidity or temperature for a pro-
longed period.
b. Low humidity during hatching.
c. High temperature during hatching.
d. Nutritional deficiencies.
e. Breeder diseases.
f. Poor ventilation.
g. Inadequate turning during first 12 days.
h. Injury during transfer.
i. Prolonged egg storage.

9. Sign: Shell partially pipped, embryo alive
or dead.

Causes:
a. See 8.a-i.
b. Excessive fumigation during hatching.
c. Eggs set small end up.

10. Sign: Chicks hatch early; tendency to be
thin and noisy.

Causes:
a. Small eggs.
b. Differences among breeds.
c. Incubator temperature too high.
d. Incubator humidity too low.








11. Sign: Chicks hatch late.


Causes:
a. Large eggs.
b. Old breeders.
c. Eggs stored too long (40 min. increase in
incubation time/day of storage, .5% to 1.2%
decrease in number hatched/day of storage).
d. Incubator temperature too low.
e. Weak embryos.
f. Inbreeding.
g. Incubator humidity too high.

12. Sign: Slow, protracted (drawn-out) hatch.

Causes:
a. Mix in the incubator of eggs stored for long
and short periods (1.2% loss of hatch/day of
storage when all eggs set at the same time;
only .5% loss/day when eggs stored for long
periods are set earlier to allow a longer
incubation period).
b. Mix of eggs from young and old breeders.
c. Mix of large and small eggs.
d. Improper egg handling.
e. Hot or cold spots in incubator or hatcher.
f. Incubator or hatcher temperature too high
or too low.
g. Room ventilation system improper; high
positive pressure or low negative pressure.
Such pressures may alter incubator or
hatcher ventilation.

13. Sign: Trays not uniform in hatch or
chick quality.

Causes:
a. Mix of large and small eggs.
b. Mix of eggs from young and old breeders.
c. Mix of eggs from different strains or breeds.
d. Some eggs stored much longer.
e. Lack of uniform ventilation in setter or
hatcher.
f. Disease or other stress in one or more
breeder flocks.
g. Variation in egg storage procedures among
flocks.


14. Sign: Sticky chicks; chicks smeared with
albumen.

Causes:
a. Low incubation temperature.
b. High incubation humidity.
c. Improper turning. This results in reduced
embryonic membrane growth and reduced
nutrient absorption.
d. Old eggs.
e. Very large eggs.

15. Sign: Chicks stuck in shell, dry; chicks with
shell fragments stuck to down feathers.

Causes:
a. Humidity too low during egg storage,
incubation, and/or hatching.
b. Improper egg turning.
c. Cracked eggs or poor shell quality.

16. Sign: Premature hatching; bloody navels.

Causes:
a. Incubator and/or hatcher temperature
too high.

17. Sign: Small chicks.

Causes:
a. Small eggs.
b. Low humidity during egg storage and/or
incubation.
c. High incubation temperature.
d. High altitude. Hatcheries at high altitudes
(>1,500 m or 4,920 ft) may need to adjust
for low humidity, carbon dioxide, and oxygen.
Atmospheric pressure <600 mmHg (-1,830 m
or 6,004 ft) reduces growth and metabolic
rate, increases loss of water from the egg.
e. Thin, porous shells.

18. Sign: Unhealed navel; dry, rough down
feathers.

Causes:
a. High incubator temperature or wide fluctua-
tions in temperature.
b. Low temperature in hatcher.
c. Humidity too high in hatcher or not lowered
when hatching complete.
d. Inadequate breeder nutrition.








19. Sign: Unhealed navel, wet, odorous;
mushy, large, soft-bodied, and lethargic
chick.

Causes:
a. Omphalitis (navel infection). Contamination
from dirty trays, unsanitary machines or
hatchery, dirty eggs, inadequate egg sanita-
tion or fumigation.
b. Low incubator temperature.
c. High incubator or hatcher humidity.
d. Inadequate ventilation.

20. Sign: Weak chicks.

Causes:
a. High hatcher temperature.
b. Poor hatcher ventilation.
c. Excessive fumigation.
d. Contamination.

21. Sign: Chicks malpositioned. Normal
position after 19 days of incubation:
embryo's long axis same as long axis of egg;
head in large end of egg; head to the right
and under right wing; beak toward air cell;
feet toward head.

Causes:
a. Eggs set small end up or in horizontal
position.
b. Inadequate or improper turning.
c. High or low incubator temperature.
d. High humidity.
e. Old breeders.
f. Round-shaped eggs or very large eggs.
g. Nutritional deficiencies, especially vitamin A
and vitamin B12.
h. Eggs handled or stored improperly.
i. Retarded development.

Embryos <18 days old may be in a position
different from that for hatching but one
normal for their age (for example, the head-
between-thighs position). The feet-over-head
position is hard to distinguish and may be
normal. The beak-over-wing position is prob-
ably a normal variant. Some malpositions
are lethal; others are not.


22. Sign: Malformations.

Causes:
a. Improper egg storage.
b. Jarring of eggs or transporting large end
down.
c. Heredity.
d. Nutritional deficiencies, e.g., biotin, riboflavin,
zinc, or manganese.
e. Inadequate turning.
f. Improper egg orientation, e.g., small end up.
g. High or low incubator temperature.
h. Breeder diseases.
i. Inadequate ventilation or shells with low
porosity or permeability.

23. Sign: Crooked toes, spraddled legs.

Causes:
a. High or low incubator temperature.
b. Inadequate nutrition.
c. Smooth bottom hatching trays.

24. Sign: Short down, wiry down.

Causes:
a. Nutritional deficiencies, especially riboflavin.
b. Mycotoxins and other toxic or inhibitory sub-
stances, resulting in nutritional deficiencies.
c. High incubation temperature during days
1 to 14.

25. Sign: Eyes closed, down stuck to eyes.

Causes:
a. Temperature too high in hatcher.
b. Humidity too low in hatcher.
c. Down collectors inadequate.
d. Chicks remain in hatcher too long after
hatching.
e. Excessive air movement in hatcher.

26. Sign: Exploders.

Causes:
a. Dirty eggs from nest. Dirty nests.
b. Floor eggs.
c. Eggs improperly washed; eggs wiped or
cleaned with contaminated cloth or buffer.
d. Dust from breeder house, cooler, transport, etc.
e. Water condensation on eggs (sweating).








f. Water sprayed, fogged, or splashed on eggs;
eggs dipped in contaminated solutions.
g. Contamination from earlier exploders,
leakers, or broken eggs.
h. Contamination from handling eggs with dirty
hands or equipment.
i. Contaminated setter flats, air filters, water
(humidity) system.

27. Sign: Dwarf embryos: runts in growing
chicks.

Causes:
a. Egg contamination.
b. Hatchery contamination, especially during
hatching.
c. Breeder diseases.
d. Heredity.
e. Nutritional deficiencies.
f. Thyroid abnormalities.

28. Sign: Crossed beak, twisted beak.

Causes:
a. Heredity.

29. Sign: Missing eye(s), other eye
abnormalities.

Causes:
a. High incubator temperature during days
1 to 6.
b. Low oxygen during days 1 to 6.

30. Sign: Exposed brain.

Causes:
a. High incubator temperature during days
1to 3.
b. Low oxygen during days 1 to 3.

31. Sign: Red hocks in hatched chicks or
unhatched pips.

Causes:
a. Prolonged pushing on shell during pipping and
hatching.
b. Vitamin deficiencies.
c. Thick shells, as in pullet flocks.
d. High incubator humidity and/or low incubator
temperature.


32. Sign: Small air cell, broad pip area,
membrane incompletely cut, red hocks,
edematous chick, unabsorbed albumen,
yolk incompletely retracted, egg weight
loss <10%.

Causes:
a. High incubator humidity.
b. Very thick shells, as in pullet flocks.
c. Low incubator temperature.

33. Sign: Micromelia (shortened long bones,
parrot beak, bent bones); chondrodystro-
phy (similar to micromelia).

Causes:
a. Heredity, lethal genes.
b. Nutritional deficiencies (biotin or manga-
nese).

34. Sign: Short beak, missing beak, face
abnormalities.

Causes:
a. Incubator temperature too high during days
1to 5.
b. Heredity, lethal genes.
c. Developmental accidents.
d. Nutritional deficiencies (niacin).

35. Sign: Ectopic (exposed) viscera.

Causes:
a. Incubator temperature too high.
b. Heredity, lethal genes.

36. Sign: Hemorrhage.

Causes:
a. Red skin incubator or hatcher tempera-
ture too high.
b. Bleeding in chorioallantois rough
handling at transfer.
c. Nutritional deficiencies (vitamin K or
vitamin E).
d. Embryos that died at days 11 to 15 and
appear small and dark red usually caused
by molds or other contamination.








37. Sign: Swollen head and back of neck
exudativee diathesis increased capillary
permeability).

Causes:
a. Nutritional deficiencies vitamin E or
selenium.

38. Nutritional deficiencies and toxicities;
almost always a breeder flock problem.

Vitamin A:
Circulatory system development abnormal;
skeletal abnormalities, especially in the skull
and spinal column; degenerative changes in
the brain, spinal cord, and nerves; embryonic
mortality is early (during days 2 to 3). Chicks
hatching may have watery discharge from
eyes or have eyelids stuck together. A great
excess of vitamin A also will cause skeletal
abnormalities.

Vitamin D3:
Late embryonic mortality (>17 days); stunting;
poor skeletal growth; rickets.

Vitamin E:
Circulatory system problems, exudative
diathesis, hemorrhages, stunting, encephalo-
malacia, eye abnormalities (e.g., cloudy lens
or hemorrhages), edema of neck and feet;
embryonic mortality peaks during days 2 to 5.
Muscular weakness after hatching.

Vitamin K:
Hemorrhages in embryo and membranes,
especially at or near time of hatching.

Thiamin:
Polyneuritis; early mortality peak and late peak
219 days; many dead chicks in hatching trays.

Riboflavin:
Stunting, short legs, disorganization of the
circulatory system, edema, clubbed down, curled
toes, micromelia, anemia, brown or dark green
liver; mortality peaks during days 3 to 5, 10 to
15, and 21 to 22. Mortality peaks change from
late to early as breeder depletion of riboflavin
proceeds.

Niacin:
Hypoplasia (decreased growth and development)
of skeletal muscles, edema, short upper beak,
nervous and vascular system abnormalities.
Mortality peaks during days 8 to 14.


Vitamin B, (pyridoxine):
Inhibition of early embryonic growth; mortality
peaks during days 8 to 14.

Pantothenic acid:
Subcutaneous hemorrhages, edema,
hydrocephalus, poor feathering, twisted legs,
fatty livers, opacities of the eye, pale, dilated
hearts; embryonic mortality peaks during days
2 to 4 and 11 to 15.

Biotin:
Chondrodystrophy and micromelia (deformed
skeleton, shortened long bones, parrot beak),
syndactylism (webbing between toes); hemor-
rhages in the embryo and chorioallantois; peak
embryonic mortality during days 3 to 4 and 217.
The early mortality peak is greatest with severe
deficiency, while the late peak is greatest with
mild deficiency.

Folic acid:
Bent tibia, syndactylism (toe webbing), flattened
head, small eyes, exposed viscera, parrot beak,
other beak defects, stunting; peak embryonic
mortality days >17.

Vitamin B1:
Edema (especially around eyes), hemorrhages,
curled toes, short beak, poor leg muscle develop-
ment, dwarfing, fatty liver, enlarged thyroid,
dilated, irregularly shaped heart, head-between-
thighs malposition; peak embryonic mortality
during days 8 to 14 (small peak) and 16 to 18.

Manganese:
Chondrodystrophy, deformed skeleton, shortened
long bones, parrot beak, micromelia, edema,
abnormal down feathers; peak embryonic mortal-
ity days >18. Chicks uncoordinated.

Zinc:
Skeletal defects, especially in posterior vertebral
column (most common defect is rumplessness),
small eyes, exposed viscera, beak and head
abnormalities, edema. Chicks are weak; will
not stand, eat, or drink. Embryonic mortality
can be very high.

Calcium:
Effects more indirect through poor shell quality,
increased egg weight loss, and increased con-
tamination. Stunted growth, decreased bone
development, and increased mortality tend to
occur in later stages. A great excess of calcium
also will cause embryonic abnormalities.








Magnesium:
Nervous tremor, gasping, and convulsions at
hatching.

Phosphorus:
Abnormal bone formation, stunting; mortality
peaks during days 14 to 16.

Copper:
Blood and circulatory system defects. Mortality
peaks during days <3.

Iodine:
Affects thyroid activity. Deficiency or excess
causes increased incubation time, decreased
growth, and increased mortality. Thyroid
may be enlarged.

Selenium:
Exudative diathesis; selenium will spare vita-
min E. Very high levels of selenium are toxic:
edema of head and neck, twisted legs, necrosis
in brain and spinal cord, short upper beak,
missing eyes, protruding eyes, an increase in
malpositions.

Molybdenum:
>17 ppm in the egg results in 100% mortality by
day 12.

Lithium:
Excess causes high embryonic mortality associ-
ated with inhibited development, eye defects,
enlarged aorta, abnormal neural tube.

Boron:
Excess boron in egg (44 ppm) causes embryonic
mortality in early development and at day 13.
Abnormalities similar to those ofriboflavin
deficiency. Face, beak, and appendicular skel-
eton abnormalities.

Protein, amino acids:
Deficiency, excess, or imbalance of some amino
acids can cause embryonic abnormalities and
mortality. Abnormalities include small or
abnormal upper and/or lower beak, disorganized
protrusions in the brain, exposed viscera,
twisted and shortened limbs, twisted spine,
short body, degeneration of the eye.

Fat, fatty acids:
Linoleic acid deficiency: slow development,
75% of embryos in the head-over-right-wing
malposition; mortality peaks during days 1 to 4,
8 to 14, and >21. Lipid transfer from the yolk


to the embryo is reduced in the first few eggs
produced by young pullets; this appears to
result in increased embryonic mortality.

39. Miscellaneous substances:

Tetracyclines:
Inhibition of skeletal mineralization, erosion of
long-bone cartilage, skeleton malformation.

Sulfanilamides:
Retarded growth, shortened long bones,
extreme micromelia, parrot beak, rumplessness.

Penicillin:
Edema and hemorrhage in wings, legs, and head.

Aflatoxin BI:
Stunting (beginning at day 12), small liver, high
mortality.

Ammonia (in incubators):
No closure of neural tube, mortality.

40. Microorganisms:

Infectious bronchitis:
Stunting, retarded lung development, small
heart, enlarged spleen. Small chick resulting
from thin, porous shell and excessive water loss.

Newcastle disease:
Reduced growth, small amnion, abnormalities
in neural and sensory tissues in early embryo.

Botulism:
Muscle atrophy, fat accumulation, joint prob-
lems, short upper beak.

Staphylococcus:
Extensive hemorrhages and tissue damage.

Streptococcus:
Destruction of the synovial lining of the joints.

E. coli:
Rots.

Aspergillus:
Black or dark green rots. Embryo red or dark,
dwarfed.

S. pullorum, S. gallinarum, and
S. typhimurium:
Egg transmitted. Embryonic septicemia, high
embryonic mortality, high chick mortality.









Landmarks of embryonic
development

Before oviposition:

Ovulation First meiotic division of
oogenesis.
30 min. post-ovulation Second meiotic
division and fertilization.
4 h post-ovulation First embryonic
division.
4.3 h post-ovulation Second embryonic
division.
5.5 h post-ovulation Third division.
6.3 h post-ovulation Fourth division.
6.4 to about 25.5 h post-ovulation (oviposition)
Continued division and growth; cells segre-
gate into groups for special functions. Several
hundred cells at oviposition.
Between oviposition and incubation -
No growth; embryo is inactive (if embryo is
held below 76F or 25.50C, which is physiologi-
cal zero); normal storage temperature is 550
to 650F or 130 to 180C.

During incubation:

Day 1:
6 to 10 h- First kidney-like cells (pronephros)
begin to form.
8 h- Appearance of primitive streak.
10 h Yolk sac (embryonic membrane)
begins. Functions include: a) blood
formation; b) yolk digestion; c) yolk
absorption; d) food provision after
hatching. Mesoderm appears;
embryo oriented at 90 angle to
egg's long axis; mesonephros begins.
18 h Primitive gut begins; primordial
germ cells appear in germinal
crescent.


20 h -
21 h-


Vertebral column begins.
Appearance of neural groove,
nervous system.


22 h Appearance of first pair of somites
(block-like segments) and head.
23 to 24 h- Blood islands, vitelline (yolk sac)
circulation, blood, heart, blood ves-
sels begin (2 to 4 somites).


Day 2:
25 h Appearance of eye; vertebral column
visible; embryo begins to turn on left
side (6 somites).
28 h Ear begins (7 somites).
30 h Amnion (embryonic membrane
around embryo) begins. Primary
function is to protect embryo against
shock and sticking; also responsible
for some albumen absorption.
Chorion (embryonic membrane that
fuses with allantois) begins; heart-
beat begins (10 somites).
38 h Cranial flexure and torsion evident;
heartbeat moves blood (16 to 17
somites).
42 h Thyroid begins.
48 h Anterior pituitary and pineal glands
begin to develop.

Day 3:
50 h Embryo turns on left side; allantois
(embryonic membrane that fuses
with chorion) begins. Functions of
chorioallantois are: a) respiration;
b) albumen absorption; c) absorption
of calcium from shell; d) storage of
kidney excretions.
60 h Nasal pits, pharynx, lungs, anterior
limb buds begin.
62 h Posterior limb buds begin.
72 h Middle and outer ear, trachea begin;
amnion completes growth around
embryo.

Day 4:
Tongue and esophagus begin; embryo separates
from yolk sac; allantois grows through amnion;
contractions occur in amnion wall; adrenal
development begins; pronephros (nonfunctional
kidney) disappears; metanephros (definitive or
final kidney) begins; proven-triculus, gizzard,
ceca, large intestine begin. Pigment visible in
eye (dark eye).

Day 5:
Reproductive system and differentiation of sex
appear; thymus, bursa of Fabricius, duodenal
loop begin; chorion and allantois begin to fuse;
mesonephros begins to function; first cartilage
present.








Day 6:
Beak appears; voluntary movement begins;
chorioallantois (chorion fused with allantois)
lies against shell near large end of egg.

Day 7:
Digits appear; comb growth begins; egg tooth
begins; melanin produced; absorption of min-
eral from shell begins. Chorioallantois is
attached to inner shell membrane and growth
around the inner surface is progressing.

Day 8:
Father tracts appear; parathyroid begins; bone
calcification begins.

Day 9:
Growth of chorioallantois about 80% complete
(still open at small end); mouth opening
appears.

Day 10:
Beak begins to harden; digits completely
separated.

Day 11:
Abdominal walls established; loops of intestine
begin to protrude into the yolk sac; down feath-
ers visible; comb and wattles visible; claws and
scales appear on toes; mesonephros reaches
maximum level of function, then begins to
degenerate; metanephros begins to function.

Day 12:
Chorioallantois completes enclosure of egg con-
tents; embryo water content begins to decrease.

Day 13:
Cartilaginous skeleton is relatively complete;
embryo heat production and oxygen consump-
tion begin to increase rapidly.

Day 14:
Embryo begins to turn head toward large end
of egg; long bone ossification becomes rapid.
Turning of egg no longer essential.

Day 15:
Intestinal loops easily seen in yolk sac;
contraction of amnion ceases.


Day 16:
Beak, claws, and scales relatively cornified;
albumen is practically gone and yolk increas-
ingly important as food source; down feathers
cover body; intestinal loops begin to retract
into body.

Day 17:
Amniotic fluid decreases; embryo positioning
head toward large end, toward right wing with
beak toward air cell; definitive feathers begin.

Day 18:
Blood volume decreases, total blood hemoglobin
decreases. Embryo should be in proper position
to hatch: embryo's long axis the same as long
axis of egg; head in large end of egg; head to
right and under right wing; beak pointed
toward air cell; feet toward head.

Day 19:
Intestinal loop retraction complete; yolk sac
begins to enter body cavity; amniotic fluid
(swallowed by embryo) disappears; beak may
pierce air cell and lungs begin to function
(pulmonary respiration).

Day 20:
Yolk sac completely drawn into body; air cell
pierced, followed by functioning of pulmonary
respiration; embryo makes sounds; chorioallan-
toic circulation, respiration, and absorption
decrease; embryo may pip shell.

Day 21:
Hatching process: chorioallantoic circulation
ceases; embryo breaks shell over air cell
with egg tooth; embryo slowly rotates in egg
counterclockwise, chipping and breaking
shell as it does; embryo kicks and attempts
to straighten neck, pushes shell open; kicks
free of shell, rests, straightens, dries.

>Day 21:
Some embryos are unable to hatch but survive
beyond the normal hatching time.

Developmental stages of other avian species
can be estimated by comparing with those of
the chicken on the basis of percentage of incubc-
tion time.









Hatching egg breakout


A breakout analysis of hatching eggs must be
done to evaluate the breeder flock's progress with
respect to fertility and hatchability. It is an abso-
lutely essential diagnostic tool for identifying the
causes) of problems in hatchability. Three types
of breakout are advantageous in evaluation and
problem analysis. These are: (1) breakout of fresh,
nonincubated hatching eggs; (2) candling of eggs
incubated for 5 to 12 days, breakout of nonviable
eggs, and recording of eggs set small end up; and
(3) breakout of eggs that did not hatch (hatch
residue).

Breakout of fresh eggs is used to provide an
immediate evaluation of flock fertility and to
confirm fertility estimated from hatch residue
breakout and candling between 5 and 12 days of
incubation. The breakout following candling will
include eggs determined to be infertile, eggs con-
taining early dead, and cracked eggs. The hatch
residue breakout includes all eggs that did not
hatch. Candle breakout and residue breakout
should be done weekly or at least every 3 weeks.
Regular, consistent analysis of these breakouts
will result in flock histories that can be used to
diagnose hatchability problems, minimize losses,
and compare strains, flocks, farms, hatcheries,
and many other variables.

Sample selection and size are important
for obtaining valid results from the breakouts.
Samples should be selected to include eggs from
representative locations in setters and hatchers for
each flock at each sampling time. Suggested mini-
mums for sample size include: (1) 10 unhatched
eggs from 5 hatcher trays; (2) all unhatched eggs
from 4 hatcher trays per setter or hatcher; (3) all
unhatched eggs from 1,000 set eggs; as well as
many others.

Records should include, but not be limited to,
the following variables: flock, strain, farm, date set,
machines) used, location of eggs in machine, num-
ber of eggs set, number of fertile eggs, number of
early dead (0 to 7 days), number of middle dead
(8 to 14 days), number of late dead (embryos 15
days or older), age of each embryo, malpositions
(in embryos 19 days or older), number pipping,
malformations, number of eggs contaminated (rots),
number of cracked eggs (transfer cracks and
others), unusual egg traits (size, shape, shell qual-
ity, cleanliness), number of dead and culled chicks,


and number of live chicks. Clear, accurate records
are essential for useful egg breakout analysis.

Eggs should be removed from the hatcher tray,
placed on egg flats, and identified as to flock, loca-
tion, etc. The exterior of the egg is examined first
for egg traits, pipping, and location of the air cell.
The shell is cracked at the large end, over the air
cell, and a hole opened in the shell and membranes
to observe the interior of the egg. If the egg ap-
pears to be infertile or contains a very early dead
embryo, the germinal disc must be located to make
a definitive identification of fertility. If the embryo
is relatively small, the egg can be broken into a
dish for further examination. Eggs with late-stage
embryos should be observed for pipping into the
air cell, then opened with tweezers or scissors
from large end to small end without disturbing the
position of the embryo. The embryo's position (see
earlier discussion on positions), the embryo's age
(see section on development stages), malformations,
contamination, and other factors should be ob-
served and recorded. Comparisons with live
embryos of various ages can be used to train those
developing experience in the breakout technique.


References

Abbott, U. K. 1975. Identifying causes of prob-
lems in hatchability. Poultry Digest
(November): 446-47.

Anonymous. 1971. Incubation trouble shoot-
ing. Denver: Robbins Incubator
Company.

Anonymous. 1991. Hatchery trouble shooting
guide. Glastonbury, Conn.: Arbor Acres,
Inc.

Coleman, M. A. 1986. Solving hatchability
problems. Poultry International (Decem-
ber): 12-15.

Hodgetts, B. 1988. Why do your embryos die?
Internat. Hatchery Practice 2 (3): 4, 5,
7,9.

Hodgetts, B. Solving hatchability problems.
Information for flock farms and hatcher-
ies. ADAS Ministry of Agriculture, Fish-
eries and Food. Wolverhampton, UK.









Landauer, W. 1967. The hatchability of
chicken eggs as influenced by environ-
ment and heredity. Monograph I (Re-
vised). Storrs Agricultural Experiment
Station, Conn.

McDaniel, G. R. 1990. Hatchability: Many
factors affect results. Poultry Digest 49
(9): 20, 22, 24, 28, 30.

North, M. 0., and D. D. Bell. 1990. Commer-
cial chicken production manual, 103-34.
New York: Van Nostrand Reinhold.

Patten, B. M. 1964. Foundations of embryol-
ogy. 2d ed. New York: McGraw-Hill,
Inc.

Romanoff, A. L. 1960. The avian embryo.
New York: The MacMillan Company.

Romanoff, A. L., and A. J. Romanoff. 1972.
Pathogenesis of the avian embryo.
New York: Wiley-Interscience.


Tullett, S. G., and R. C. Noble. 1989. Under-
standing the chick embryo (III). Low
hatchability problems in young parent
stock. Misset International Poultry
(January): 8-9.

Wilson, H. R. 1991. "Physiological require-
ments of the developing embryo:
Temperature and turning." In Avian in-
cubation, ed. S.G. Tullett, 145-56. Devel-
oped from Poultry Science Symposium
Number Twenty-Two. London:
Butterworth-Heinemann.

Wilson, J. L. 1991. Hatching egg breakout
methods are explained. Poultry Digest
50 (9): 20, 22, 24, 25.

Wineland, M. J., and J. T. Brake. 1984.
Trouble-shooting fertility and hatchabil-
ity problems. PS&T Guide No. 34.
North Carolina Agricultural Extension
Service.


Summers, J. D., and S. Leeson. 1985. Poultry
nutrition handbook, 119-24. University
of Guelph, Canada: Department of
Animal and Poultry Science.
























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