’l

I

1

WW)"

W

h

l

I

I ’ ‘1‘,

l
v

I

)I H I,

’f

I

l I,

 

AN ANALYS‘S OF 31V! YEARS
{)F :QREEDWG FOR UVABILITY
{N RHODE ISLAND REDS

fixed: far {he Deena @f M. 3.
MICHSGAN STATE COLLEGE
Mannen Gram McPherson

39619

THESIS

This is to certifg that the

thesis entitled

"An Analysis of Five Years of Breeding
For Livability in Rhode Island Reds"

presented bl]

Harmon G. McPherson

has been accepted towards fulfillment

of the requirements for

Master of Sciegce degree: in Poultrr Husbandry

 

'u
g

“I I ‘7) i A -- 1., 1.- k- (- 4»
Majm' [trquSSnI‘

Date Jm 2. 1%9

0169

 

AN ANALXSIS OF FIVE YEARS

OF BREEDING FOR LIVABILITY IN RHODE ISLAND REDS

BY

Mannon Greer mofihgrson

A.THESIS

Submitted to the School of Graduate Studies of Michigan
State College of Agriculture and Applied Science
in partial fulfillment of the requirements

for the degree of
MASTER OF SCIENCE

Department of Poultry.Husbandry

1 9 h 9

TABLE OF CONTENTS

Acknowledgement . . . . o . . .
Introduction . . . . . . . . .

The mortality Problem . .

Types of Poultry'Farms . .

Classification of Diseases
Purpose . . . . . . . . . . . .
Review of Literature . o o . .
Procedure . . . . . . . . . . .
Results . . . . . . . . . . . .
Discussion . . . . . . . . . .
Conclusions . . . . . . . . . .

Bibliography

Appendix 00000000000

13-18333

Page

ACKNOWLEDGMENT

The writer wishes to take this opportunity
to express his appreciation to Professor J. A.
Davidson of the Poultry Department of Michigan
State College for his assistance and encouragement

in preparing this paper.

INTRODUCTION

The Mbrtality Problem

 

Heavy loss from.disease is recognized as one of the limiting
factors in the poultry business throughout the entire United States.

The economic importance of high mortality is summarized in several books
(h) (31), and in many’PubliShed articles (1) (2) (5) (25) (3h) (37)-

The greatest losses occur among pullets during their first year of laying
and it is this phase of the problem.that is receiving the most attention

from.investigators.

Darrah (l6) summarized the mortality records of 1073 N. I. State
poultry farms from 1926 to l9hl and reported as follows: "The death rate
of chicks has dropped considerably. In the early 1930's, about 25 chicks
died out of every 100 started. In l9hl, only about 15 chicks died out of
each 100 started. The average death rate in the laying flocks remains as
high today as it was a dozen years ago. Studies of commercial poultry
farms in the early 1930's showed that about 2h layers died out of each
100 kept during the year. In a l9hl study, 25 died out of each 100 kept!

Darrah showed the effect of mortality on the income of H. I. State

poultry farms in table 1. (16).

Table 1.
Relation between Death Rate and Labor Income

(1073 N. I. State Poultry Farm Records, 1926 to l9hl)

Death Rate Labor Income
Low (11%) $1620
Medium.(22%) 1330

High (h3%) 880
Types of Poultry Farms

The development of strains of domestic fowl resistant to disease
is beginning to play a major role in the disease control program of the
poultry industry. For this reason, the various kinds of poultry enter-
prises and their relation to the disease control program should be under-
stood. The U. S. Agricultural Census, l9h0, gives the following dis-

tribution of chickens in the United States:

Table 2.
Size of flock Average No. Percent of all Chickens
per flock Group Cumulative
Under 50 23 20.6 20.6
50-99 63 20.9 h1.5
100-199 126 27.h 68.9
200-399 2&2 16.9 85.8
too-799 h99 6.h 92.2
800-1599 IOhS h.0 96.2
1600-3199 2136 2.3 98.5
3200& over 5573 1.5 100.0

Over eighty five percent of the chickens in the United States
are in flocks of less than hOO. Only Threeweight tenths percent are
in flocks as large as 1600 chickens. Mbst of the farms which keep
small numbers of chickens, and many which keep large numbers, do not
hatch their own chicks. Chicks to maintain theseflocks are purchased
from hatcheries or from poultry farms which sell chicks. Darrah (16)
reported that h8 out of 100 commercial poultry farms in N. I. State
sold chicks in 19hl.

Commercial egg farms keep from one thousand to many thousands of
laying birds and depend on the sale of eggs as their main source of income.
Mbst commercial egg farms buy chicks to maintain their laying flocks and
they'replace from seventy five percent to one hundred percent of their
birds each year. This type of poultry farm.has shown a rapid increase
in recent years near centers of population.

Commercial hatcheries are the main source of chicks for the small
flocks and the commercial egg farms. They have shown a rapid increase
in both numbers and capacity since 1930. Hartman.and Vickers (29) quote
figures from the U.S.D.A. Bureau of Economics Hatchery Reports which
show an increase from 671 million chicks hatched in 1930 to 1,620 million
in l9h5. In 1930, seventy'percent of all chicks hatched were hatched in
commercial hatcheries, and in l9hS, the percent had increases to eighty»
eight &.six tenths percent. Hatcheries,for the most part, own few or no

chickens. Eggs for hatching are purchased from small flock owners and

from commercial egg farms.

->-

Poultry breeding farms are few in number compared to the other
kinds of poultry farms, but they hold a strategic position in the
industry. They depend on the sale of baby chicks, hatching eggs, and
breeding stock of superior quality as their source of income, rather
than market eggs and meat.

In the interrelationship of these various kinds of poultry
enterprises probably lies the key which might explain the great in-
crease in mortality of poultry laying flocks. If we could determine
exactly the cause, we might have an effective aid in finding a rem!
edy. The increase in poultry mortality since 1925 has been concurrent
with the rapid increase of the hatchery business. Whether there is
any relation between the two is problematical, but the increased use of
hatchery chicks has certainly resulted in a wider spread of gemetic and
pathological factors favorable to the development of disease. The
widespread exchange of chicks between different parts of the nation has
brought chicks in contact with disease producing agents of a different
nature, type and virulence from those of the environment of their
parents. To the extent that natural and artificial selection may have
developed genetic resistance in chickens which were previously kept with-
in a given area, the introduction of chicks from other areas may have
resulted in an ever increasing number of susceptible animals. Also
the rapid course of pathological agents through these susceptible
animals may have resulted in an increasing virulence of the organism. (8)

The use of hatchery chicks has also been accompanied by the

practice of raising chicks in larger flocks, often partly or entire-
1y indors, at all seasons of the year. It has also been accompanied
by the practice of keeping a larger percent of pullets in the flocks.
All of these things increase the number of susceptible animals. and
the number of months in the year when there are susceptible animals
present of the right age for disease organisms to perpetuate them-
selves.

Mcst hatcheries buy eggs from small flock owners and from.commercial
egg farms. Male birds are sometimes purchased from poultry breed-
ing farms for improvement purposes, or males are swapped from one farm
to another. 0n the whole, here is no long range breeding program
for improvement of resistance to disease. The practice of constant-
1y mixing stock from various sources has resulted in a great hodge-
podge of genetic characteristics which does not lend itself to
improvement by selection.

The main task of selection and breeding falls on the breeding
farms and the experiment stations. While these, too, have had their
mortality problems, most of the work at present being done in applying
genetic principles to the production of better stock is being done
on these farms and the results are encouraging. In the western
N. I. Egg Laying test in l9h5, the mortality was thirteen & five-tenths
percent, compared to twenty'four*& seven-tenths percent the year

the tests were started in 1932. (Table 3)

Table 30
& Mortality in Laying Tests
Year Chicks hatched by
Commercial Hatcheries Mich. N. J. west. N. I.
1930 671,576 18 28
1931 516,220 23 30
1932 537.351 28 22 28.7
1933 588,587 27 26 21.9
1938 525,987 28 25 21.0
1935 689,720 30 22 20.1
1936 790.789 29 28 19.5
1937 687,595 27 25 17.7
1938 785,687 25 28 16.6
1939 916,809 28 25 18.6
1980 859,381 g 15.5
1981 19093.300 12.8
1982 1,280,290
1983 1,609,121
1988 1,288,891
1985 1.620.773 13.5

The problem.of today is to get a distribution of the improved
stock from.the breeding farms, to the farms supplying hatching
eggs, to the hatcheries, and to the farms producing eggs and.meat.
waters (h?) (88) (h9) (50) has proposed a "Closed flock" plan which,
if universally adopted, should result in better production and lower
mortality for all farmers in the country.

Classification of Diseases.

The Ninth N. r. State Egg Laying Tests (1980) Listed the causes
of mortality Of 505 birds which died in the two tests in 19h0. These
have been summarized in table: h.

Table 8.

Percent mortality from various Causes
In N. Y. State Egg Laying Tests in l9h0

Cause Percent of
Total Mortality

Fowl leucosis complex 37.0

Conditions associated with

egg production 18.h
Miscellaneous 16.5
Nonspecific infections 15.8
Impactions and ruptures 7.1
Nutritional 2.2
Cannibalism ‘ 2.2
Parasites .h
Specific bacterial &.virus .h

Total 100.0

These figures are probably not representative of the average
farm.since they represent the best pullets from the best farms in the
country, and are all pullets. Data from actual farm flocks are not
available because for most deaths no positive diagnoses are made, and
many birds are culled out for health or economic reasons which would
have died if they had not been removed. The summary does serve to
emphasize the large percent of mortality due to fowl leucosis complex
and the small percent caused by Specific bacterial and virus diseases.
In any study of reduction of mortality by the application of gentic

principles this is of considerable importance.

Beach (6) studied the autopsies of 9,526 birds which died or

were culled from the University of California. poultry husbandry flock,

andh,776 autopsies of birds from California poultry farm flocks and found

non-specific disease conditions responsible for sixty two &.five tenths perount

of the loss from the University flock and fifty nine & eight tenths percent

of the California farm flocks.

diseases is shown in table 5.

Table 5

The distribution of the nonspecific

Percent and Distribution Nonspecific Diseases

California
% Mbrb % of Total
tality' mortality
due to non-
specific
Poultry'Hus-
bandry flock 22.7 62.5
Poultry farm '
flocks h6.5 59.8

Distribution of nonspecific

Alimen- Urin~ Repro- Misc.

tary' ary ductive
28.0 15.7 39.2 16.9
32.6 19.2 31.2 16.9

The group of diseases included in the "avian leucosis complex"

is classified in a report from the U. 5. Regional Laboratory, East

Lansing, Mich., as follows:

Lymphomatosis

Neural
Ocular

Visceral

Osteotropic

-10-

Blood forms
' Erythroblastosis
Granuloblastosis
Myelocytomatosis
Sarcoma and other tumors

methods of Disease Control

General sanitation is the method of disease control most
commonly recommended to poultry raisers. ,A review of this subject is
given by Martin (8) and by Van Es and 01ney (h5). ,As a prac-
tical means of controlling disease, the value of sanitary practices is
limited to those diseases which are spread by the environment of the
house and ground, and these are a relatively small percent of the
total mortality of adult stock. Hutt (26) summarized the deaths of
1,922 birds which died in the N. 1. State Egg Laying tests between
1931 and 1937 and stated that thirty eight percent of the deaths
were due to neoplasms, and eighty seven percent of all deaths were
caused by diseases which could not be controlled by generally
recommended sanitary practices.

Certain management practices are also related to disease con-
trol. The recommendation is to raise chicks in small flocks, well
spread out on the land, not over 600 pallets per acre. This mainp
tains a biological balance between the infective agents and the
number of susceptible chicks. The practice of rotating ranges is an

effective control of coccidiosis and worms.

Kennard (32) and Hutt (27) presented evidence that pullets sur-
vive better as layers when they are raised on the ground far enough
away from mature stock to prevent infection during the first few weeks
of age. Raising young stock in confinement or on wire reduces mor-
tality during the growing period but does not increase their survival
rate as layers, under ordinary laying house conditions. The practice
of having all-pullet flocks reduces mortality by preventing infection
from old birds, which are carriers, to young birds.

An effective means is at hand for eradicating pullorum disease
from poultry of the United States by use of the agglutination test and
the removal of infected birds. Tuberculosis could probably be eradicated
by means of the tuberculin test.

Chickens can be successfully immunized against two specific
virus diseases, fowl pox and laryngotracheitis, and recent work in New
Jersey indicates success in the development of a vaccine against New
Castle disease. Th‘ effectiveness of the vaccines has been well estab-
lished (10) but there is still some question as to the propriety of their
unrestricted sale and use.

Recent advances in the knowledge of nutrition will undoubtedly
be an aid to poultry farmers in reducing mortality by establishing
mutritional requirements, and aiding feed manufacturers to furnish feeds
which meet the birds' needs for vitamins, amino acids, and min rals

under close confinement (hh).

A system of complete quarantine which would isolate individual
farms from outside sources of infection is very difficult to apply, but
combined with waters "closed flock" system of breeding, which would
improve genetic uniformity, it might be a practical way of reducing the
high mortality rate.

There are few medicines of value in treating diseases of poultry,
Round worms can be controlled by medication. Sulphur and some sulpha
drugs have preventive value against coccidiosis. Sulphathiazole is
useful in the treatment of coryza. Outside of these, medicine is of
little value, yet farmers place their chief reliance in cures and
annually spend millions of dollars for dopes and medicines (h5).

The field which holds the greatest promise for the reduction of
mortality in chickens is in the field of genetics. The application of
genetic principles to the production of strains with livability and
with resistance to disease shows considerable promise. Roberts and
Card (38) in 1926, were able to produce strains with resistance to
pullorum.disease, and Doyle (19), in 1928, noticed differences among
strains in resistance to fowl paralysis. Lambert and Knox (3h) bred
strains with resistance to fowl cholera. The nature of poultry diseases,
which are largely ne0p1asms, nonspecific infections, and organic condi-
tions such as impactions and ruptures, should be a favorable factor in

efforts to increase livability by genetic selection (8).

PURPOSE

The object of this report is to study the results of five years
of breeding which had been done.

The mortality in this flock had been reduced to a lower percent
than that generally reported, even in strains of known resistance. It
was thought desirable to learn what diseases were reduced or eliminated
and whether the changes were due to inheritance, to changes in environment,
or to chance.

Data were available to compare the mortality of young stock with
the mortality of pullets raised from the survivors, as was done by
Byrant (12). Changes in the age in days at which birds died from
various causes would be of interest.

Opportunity was also presented to compare the causes of mortality
in a flock where total mortality was exceedingly'low, with the published

data from other sources.

REVIEW OF LITERATURE

In the last few years, many reports have been made of successful
experiments to reduce mortality by selective breeding. Marble (36) was
able to reduce total mortality in White Leghorns from thirty nine
& eight tenths percent to twenty percent infive years, and in Barred
Plymouth Rocks from forty eight & seven tehths percent to twenty four .
& sixztenths percent. Sturkie (hl) reported a reduction from eighty
nine percent in unselected White Leghorns to twenty seven percent
after five years of breeding from families of greatest livablity.

Survival age of the birds which died was increased from 229 days to

-m-

363 days. Dimilar results were obtained by Gildow (21) and Bostian
and Dearstyne (9) and others.

Experiments including a susceptible line as well as a resistant
line have been conducted by several investigators. Byrant (11) in a
three year experiment, de:eloped two strains of White Leghorns which
showed a significant difference (by the chi square test) in the amount
of mortality. The resistant line mortality was twenty five & six tenths
percent and the susceptible line was thirty six:& three tenths percent.
From.unseleeted stock in which the mortality was sixty four percent,
Hutt, et a1, (25) (26) (27) produced a resistant strain in which
mortality was lowered from eighty three percent to thirty five percent
in eight years, while the susceptible line in the same period changed from.
seventy four percent to fifty three percent. Taylor, et a1, (h3)
produced strains with a significant difference in.mortality between
two lines.

Maintenance of a sus eptible stra n offers some means of off-
setting the error that might be included in conclusions drawn from
oneline only, because of changes in the amount and type of infection.

Other means of testing the genetic basis of resistance to disease
have been used. Hutt (27) compared the Cornell strains with four other
unselected strains and found the Cornell resistant line superior to
three out of four of the unselected strains for livablity, Hutt (26)
also crossed the Cornell resistant strain on males of an unrelated strain
bred for resistance. The Flprogeny had less mortality than either of

the parent strains. Hutt, in the sane report, inoculated part of one

-15..

year's chicks with fresh lymphomatosis tissue. The results were
twenty three and one tenth percent morality in the inoculated females
and thirteen percent in the controls. He concluded that natural
exposure was adequate to differentiate between the resistant and
susceptible strains.

Taylor, et a1, (83) inoculated resistant and susceptible lines.
Mortality in both lines increased but there was still a significant
difference between the two lines. Burmester (11;) stated that chickens
immunized against cell transports of lymphoid tumor strains were no
more resistant to neural and visceral lymphomatosis than uninoculated
chickens. Heisdorf (2h) was unable to differentiate between lines of
White Leghorns selected for resistance and susceptibility to neoplasms
by subcutaneous inoculation with lymphoid tissue. Placing lymphoid
tissue in the creps, eyes and nostrils resulted in a highly significant
difference.

The possibility of a leucoagglutination test to detect the pres-
ence of lymphomatosis in chickens has been nnde by gtafseth and by
Kisslin (33). Kisslin used the rapid plate method and antigen mice
from normal, strained canine lymphoctyes. Such a test, if it could be
made completely accurate, would be a great aid in genetic studies by
identifying birds with infection below the level sufficient to cause
death, and families completely free from lymphomatosis could be iden-
tified.

~16-
PROCEDURE

This report is based on the records of the Rhode Island Reds on
the poultry farm of Michigan State College. Selection of birds was
. made by J. A. Davidson on the bases of progeny test records started in
193R. Egg production, egg size and hatchability were considered
as well as mortality in making selections. A few birds were discarded
for surface color.

All of the Rhode Island Reds that were hatched from l93h to 1938
are included in this report and Mortality includes death from all causes.

There was no culling. The eggs from this group of birds were incubated
' L

with the eggs from the Barred Plymouth Rocks and the eghorns, the chicks
were reared with the other breeds and the pullets were housed in the
same house. No attempt was made to isolate the flock as a whole from
outside infection.

There were from seven to nine hatches a year, between the first
week in.February and the last week in.March . Chicks were raised in
ten by twelve colony houses, three hundred chicks per house. They were
hopper fed from.the beginning and grain was fed after ten days to
three weeks of age. Layers were fed by the "cafeteria" method, grain
and a mash concentrate.

The make up of the flock is summarized in the Appendix Tables I
and II. Fifty one hens were used for breeders in 193h and twelv;
additional new ones in 1935. One hundred daughters and twenty seven

granddaughters of the original sixty three hens were also used as

breeders. During the five years, three hundred seventy eight daughters,

-17-

four hundred ninety one granddaughters, and one hundred fifty four
great granddaughters were produced. These constitute the basis of

this report.

In l93h, the flock consisted of fifty one families whose
average size was 3.6 birds. In 1938, it consisted of forty two
families with an average size of 5.7 birds. In 193h, there were
twenty one families of four and over, which made up sixty five &
eight tenths percent of the flock. In 1938, the average size of the
families of four and over had risen to 7.6 birds and they consitituted
ninety-one percent of the flock.

The conditions under which these birds were hatched, reared and
housed approximate farm conditiins. All birds which died were autop-
spied by pathologists of Michigan State College.

Data were collected and summarized from each family for the years
l93h to 1938. This includes the number of chicks hatched, percent of
total mortality and mortality from leucosis complex to 190 days of age.
From.l90 days to 555 days of age it includes cause of death and age in
days to time of death.

The data was grouped in several ways for the sake of making
(zomparisons:

a) By calender years
b) By generations

c) Related first and second generations
d) Related second and third generations

e) Related first, second, and third generations

-18-

Comparisons were made in all these ways using all birds in the
groups, and then restricting the numbers to birds in families of four
and over. It was hoped in this way to bring out evidence of genetic
similarity. Families of four and over were used because four seemed
the smallest number possible to use as a test of a family, and to use
a larger number would reduce the number of families included to such an
extent that they would not represent the generation or year.

The comparisons were measured for significance by the "t" test-x- (h)

 

* t ‘: PL“ E1-
6‘ difference P2 - P1

5 72.0 significant at 5% level
t== >2.6 significant at 1% level
The ”t" test is adequate to measure the significance of the difference
between percentages but does not prove or disprove the validity of the
comparisons. Comparisons were made between years and between gener-
ations using for comparison:
Total mortality and mortality from leucosis, Appendix,
Tables III. a,b,c,d,e,
Percent Mortality from various groups of diseases,
Appendix, Tables IV. a,b,c,d,e,
Various groups of diseases as a percent of total mor-
tality, Appendix, Tables V. a,b,c,d,e,

Survival age in days, Appendix, Tables VI.

For convenience in summarization, the causes of mortality were

grouped under the following headings: Reproductive diseases, Digestive

diseases, leucosis complex, reSpiratory diseases, metabolic diseases,
nephritis and pertonitis, and miscellaneous diseases. The diseases
included under the various headings are shown in the Appendix, Table
VII. Nephritis and Peritonitis were at first included in the mis-
cellaneious but were later taken out and grouped together because they
so often account for a high percent of total mortality, not because of
any relationship between the two.

Correlations were determined between the mortality of chicks and the
mortality of pullets raised from the survivours, for total mortality, and

mortality from leucosis complex.
RESULTS

Total mortality in this flock was reduced to thirteen.& five :tenths
percent after five years of selection. The first year of the study it
'wes twenty three & twe tenths percent. This twenty three &.two thenths
percent is the mortality of the l93h progeny, not the mortality of the
parents. Mortality records of the parent stock before l93h were not
available.

The reduction was not consistent from.year to year ( Chart 1).

In the families of four and over, total mortality followed the same
general pattern but was about two percent less than when all birds
were considered.

When the flock is considered by generations instead of cal-

ender years, the results are shown in table 6.

 

 

 

fi fi fi - — -.
cr— —— q — -

 

 

 

 

 

 

 

 

 

 

 

 

 

  

 

 

 

 

r“. .—r*'=' : ' "I
i 1 . I
I 0 > I
: _ _ _ i
a - abut 1L . 3
Tofu l M oan l may i
5 Po [lets [go ~5¢€duys :
I ' ‘ :. . 1 ._ 1
; ‘%Mmt.mv r. i
E _ _.- 30 .. _ - «H ‘ pl
r J g
l . .
:L. . 2.5—... I
' l
9 1 i
l 3
'- _--20 x- H I
f I
! . a
:- 15:4p— - . . .
I ‘ AlLb'vaIs. j \\ I
_..... _... iTEmH-tas a} q-and‘ over. =
i- .- 10.- : _1 1 1 1 . . p _..} Y
’ may was i . (93-6 147137 . 1.9153"
. , Yeavs ~ _.
. ’ i
. . i v 'i '
' i i ' I ' ' ' 5 ‘
x___.__.__..,-_... _.1 in- -____i .I ........ --..,_!. ”_---” . __..,_ .___~_. -_ _- i.-. -. -
N _ 3.”, L. -. . .1‘1'-;;._'_..: ' i 101391 MMWY -‘ a.
pf :- ' "W112; 5 _Iqu ‘zfiquys ' I ’ . 1
'1 :: f1'_"1" . .
j - z i f . . I E III ‘
~_‘_._ «_ 5‘)— VOMOVTaIITYA¥1 ._..__ i . ’ __ , __ - ”_... _.w, ___._, “.' ' ' j r;
.- . _f _ ' I "A. '
- c _ 2.51,.-- , / c ‘ -- 1+
3 ‘ “4 \ ' i
'- - - ~——~1—O-—1-- -« -- -— .._._.._ .4 >4
- I .. 15.4.; . ,
. \ \
_....- - _- JO 4., *- A" GIV‘IS . -- M... l- .4
._ _.. .— FamIUes of a aniovev‘ .. - .. - Ruffled [SIN—1nd.
J -..._..-__.Re‘aTédfOMIUE‘lif‘l-‘I'M. W HQIQ'EEAAGLV'EFII'.
— ‘ . ' ~‘ xi Y ! I I . . 4 L
‘ 131'. 211.1. . 3*:4.
Gemexq‘hons .
'1 ; ' IX ; I

—hn -—‘—a— .

 

—20—

Table 60

Total Mortality in Percent, by Generations

Generation
Group First Second Third
A11 Birds 19.8 23.1 11.0
All birds in families of h.& over 16.8 21.0 9.5
Related 1st. & 2nd. generations
in families of h&over 18.3 21.0
Related 2nd. &.3rd. Generations
in families of h.& over 15.6 9.5
Related lst., 2nd., & 3rd,. genera-
tions in families of b.& over 17.1 28.7 12.9

In all groups, second generation mortality was higher than
first generation, and third generation was lower than either first
or second.

Changes in mortality from leucosis complex are greater and show
more consistent pattern than changes in total mortality (Chart 3).
This is especially evident when the data is arranged by generations
(chart h). In all but the related lst., 2nd., and 3rd., generations
group; the second gezeration is lower than the first and the third
is lower than the second. This one group which is the exception
contains the smallest number of birds. Here the second generation w s
a little higher than the first but the third generation was the lowest
of all thegroups.

Chick mortality, on the whole, increased over the five year

period (Charts 5 8c 6'),

 

 

 

 

   

     

 

 

 

. I1 4 I 4 .I 1 1 4 11 ‘4‘
I . u I. . u .. fl 1 .. .
. . .. . . ,.. i v
~ . w a . . w. ‘. .
. . . .. a t . _ .
u o .o . I . c o I. ~. ‘ < . . a ......
i . u . .. .0 v _ .
.. . . u . . v . . -
i I h I. I i - _ -
.- . . ._ m . . . . . . -. I
I . q ..... 1 . «I o o I I u I 4 II a. II 14 u c I I o c I I I a I .
H . . . . . .
. .l +. . .
_ . v v I 1 -.
. . w . . . _ . . I . ._
v a - 9 v . a ........... . b o o o R +
.. .. . . . . _
. . . . _ M . . u . . _ .
. . .. _ . . uI .
. . u . .. . _
-0 U I ' l y . >
. I III III III IIIII I if I l 1 \IIO....... I ., . . .. . . ..IIOIIiII II.
. . .1 I O
. _. _ 1 o . -.
c -. . . m I I _ fl
_ . . . w . . . _o q -
. I I o. a . . - . I . u. . 9 . u I . . . .. u y . I
- i _ a . .....
. c . . _ V .. u . . . w .
. . . . 8 fl. . . .. M . M 1 _- . I
I w . I 4. . . a. . _ — * I . .
a . . 3. __ - . *. . . . . I I. . i . . . . .0 i- .
t I _ . I III w. , . . . . .IqIIII‘ III! I I1 4 III p v .IIlv ...I. .IIa III YIII. A I I.OII I I + I . .Il. I91 ILfiIIE. I. . I... . I N . i
. I I . . . a *V .II. o . . a - .
. .. I * . a .. . ...... _. . .- - .
_ .. . I .I . I - . i _ . I .
_ .. . .. . .. . I I .
. a x _ . . I F .- . . . u . I ,I.
- I III 1 * . . . .. I 1T III . v 4 I (Ix? 0.1. I v . OI .. I . II VI. I .
w ‘ o . . . .I I / l u . . - . . o u
.l - . .. _ I I
_ .. . . . . ‘I I. .. . ..I . . - _ . I .
I“ . w . . _ .. . . . . . . a o I . . . _ I _ I I . I d .
f. . . . - . . . . .. _ I. . . . I . . l.» . . I . I. .. I . . .I . . . r w . I
.IIIIiIIIP. I .I. I. . I... IIIrIII I. II! .II .. .. I... 1.... III: I1-..I.. 11:... . IIIIIIII. .III. I in .II V _II. .III|,.III .I. L . I1 1 I- I- . I f IIIII
. . _. _ I. .. _ .- . . 1P I . I T*.;--.-.-.- I II III I
. I . I . . _ .4 i . .
_ I # . . . . . - .. . . .. I . . . I. _. . . . .. . I - c. i
. I . 7 I
. . . . . n . , . . I . .1 . I‘ . . u . - I . I
... -. II.-- .. . _ . . .,. . . . I. -- --.I? , I ...... .. I -.. -I..- I
l
V

 

 

I
3":
.}"_.‘“

 

l
I
I
.
...
U
.
.
A

OSIIS c’p'm
“8Y3,

.
. l
.
I-

I
. o
t.
4 ?
+5
L.
d
.
- 1
-....-
I
.. I
.
I Y‘.
i .1,.

I

 

I
'I"
...IJ.'
-——v

 

 

'votlgxnu
I

 

All I

_ c:
writes

I
I
I
.
.w.‘
.
n .

IN
819336.:
five"

 

 

' i 2 I?
.T: Y -
I .
“I
‘I’mhs

. . I
. $1 I. II I} IIIIII. .+.~ «III. N I .
. .1. . - . .- I. i

. Iv - I I. . r I I
7 ..l : _ O. .I . i

-8

n7: .
"70-!
19m».
:cfiIvr

I
l
l
.51.
ILebc
A:
i
i
. I
'1" 1 self--
I
I
~ —- —-—--- — w—w-v-v—h—b—‘na-vv' <r«--~~—--~—-+-«w—o-o—-
y,
I!

I.
If"

is. ' .

 

 

 

 

     

 

 

_---I LI. III? I . ...... ... I.

 

 

 

6c. .. ; I- 4 . . A-.. h, . H
_ -.u s H- i. 5. I, .
IIIIII. II I I -IIIIO IktIITIILYI I. ..l I f IIIIIIV'III . .. II III: I I _.. ilil IIIIIII II 11.] .I-I|.|il . . I. I.
- V .0 .o . . 1
Ifil. : 1. .. 0.. u . ._ 0+1.va
. F l . i ‘.s I . W o. q
. Ir... .. i .I .I , . In..- H 5 . 3
go” . tiara - . .l-. . ...a 111W .
- t. . . -l V . M H. u . H
. . II ._.I .--.I- T- iEWIIIS I... .- -.. I u m. .
. I. i. .1.” - -IOI I. i I .l .. Iv... .
- . ...-.6, . . . .. - _ .15. .
I - . .. .m I I ” _.M.yo.I w: -. n o. .0“ .I - _
.M . -- ll. .11 H _..... ..h IL“? I . .a ...M. run-L - If ... I _
é , _...u. . . .72.... - II .... _ I
I ....I . P I l. ...IIIIII . IIII . ... - _ . . .
‘1 II . .T'Ifilil V I I a

T...
l

 

I
I

.t-..-.

1 . .
l‘ .41.... .I . . .. c _ IJwIIIII IIIIIITII. II.
. . . . . I . - . . .

 

TI
1 .
T
_...ilI
I
I
'.
‘I
I
l
I
I
I
.-- «I»
It
I.
{i
“""‘1
I...
2
‘4‘?
I
3.
'I
I

w ‘31
_--;;;;-I

I
I

w _ _...--

 

T“
LI
I
I
I’
I

l
I
Y
I

. .
r b
.
._. -_......_. _.
. l. ., ,
I ado O
or u. o. t
.- ..f II
. .
.
Il‘ ox .+
I* *
1 r e
I . ,
. I .
b
.
' l
I
o -r“
' l
I
.
I
J
- ~.
I I , . .
- -,_¢._*_-_
. I .
. . .
v
-.-—u. _-_.
I
I
.-

 

 

 

 

f
D
u—
h»

.

«b—
!
I.-.

r-
1
’ V
.
'7—9
ItI
I
HI
1 a
II
I -
MH+-§Q~-l ...
I. .
"I’ . ..
.... . I
I 4'. n ‘
W _.
..I
- 7
r I
I
w.-.
t V
I
H‘Ik‘fi- -—-‘—‘-—q “—
+ -
v
rv-c1M7
.
v v

 

O
l
I
II. III-1- _; ;--- I --.---.- --- ”1.11;...
I
I
I
I
I

 

 

. 7
fl . I
.
. . . . . N.
I. _ ..
l .. F I. . fl
4 A 1 .. . . 1 I II I I II. I .I II II
. . 4 I . . .»IH.H . . 4. .. A. “I 10:
t h . h . .. . _. . » F - . . .
- _ a . . I . . 34.2l
_ a m ..v15u321_ _ :
.I II + ”V, I I - p . - ._ . 1 . I.+I.II.IIII.PI . I--I-I+.......I. . - r .
. a .. w . n . I I. . .k I. . . .- H
. - I u C. u .D _ I . v _
. l _ . _ u. - _ I I W _ I .- . _ u
. ~ I _
- . . I . _ . u _ . . i .
. . v . . . . . I I. p . . .II. III I IIol. .II .Ioqui - I. I. .. . .II ....... 1 IIII .. a I I I]- . . . I . e I . I I I .
I- . _ I . I .
. I . I . * . 1 I . _ .
. - . I. a I . o . . U I i .-
. . a . . ..... . l
_ . . . . . - . H . .. .. .I_ . U a I , _ m _
n I. I h I . .... . .. v o .. . H II 9.1 II ..IV.II. . .P . c .c I o . o ..... .I I cII
. . . . a _ . . . . _ . - .
_ .- w I . . . .h _ _ _.. ..H .- . a _
W . . . . m _ n . . ... a . . . . _ H . . .9
I .. ... g . I .
f I d I I I r W I- .“ _- -., L. , H . _- L H .- d a Q

 

 

 

 

I .

l I.‘ ‘P~II-—' _
. I
o

- - -o

- --J‘
O

 

 

 

20..

If.

. (211an 5'7. .
TOT“ Mow-fall'fy
Chicks [To [10 days
%HWTuI;tY V f

 

 

 

 

“_.— —-;-— L—g -;-——--—L——~o¢ -o —-————L-—————l

 

 

 

. _.---19;

  

M

 

 

 

 

D——- -. I- -
.19.... . 3-: . - 5. . - .I..- I
......I— ...;annizs afuandgovev,‘ '

-- --.5'- LI I Iii * t ~ I 1 II
I I :93 , “135—1 1936 1837 [-138 I
‘ ‘ F I Yanvs '° *

i I I! I I _ I I - I-

I I I, . I . . I. ’ - . . . f - , ' .. -

'. . l .;:. ; ' . .I: ;.:I .II; I. I a.
...... - I... - '- _- - L- -- I;I.I-;.-.- ----..I, CINDY-t 6 ---'-.....,I...I. .-.. ..l_. I. -..--..}.‘I..----..* ..
.-. ' I~ - ;_ ; ITIInI Movfdh'y; g. ., I; .; . .

‘ ‘ I . 4 ' . Chicky '-*° W? fins " r '"vfi- ‘ '.
‘ . ' ’ I .. ."". """ ' ...L’ "flfTiffi'TTIII T'irfrl—Ifi ‘r f'.' . Y I I
;; ' 'an‘hhfrr ' ‘ ' ' ' ‘ * I . ' ' .;. i I
‘7' ’L t. . LI" 131' . ' t. ' TI
.: ‘. ' ..' I g ‘l ' .l
' _ - _... __IL- -- ..--III--- ..:-_'.. - -.I
i ._
— ~~U-~ Q -— '-I

 

 

-_‘_' « \V/l ‘ -~ _. _.. _. _.J”
A” bird 3.. . \I/ I
_.IT'am'Ih'es of d! or? ‘

.. _..... Q_Rd07¢dfnmill'ts

I 1°, crime?

 

--.-..-..Bgmgd Mung. w, _
Wc’o‘f—du d?! 3H.

 

 

-; I I 12. A L .l I
lit... . mod. :5ch .
‘ ‘ '; Gcn'eva‘h' on s ‘
a .
. I
. !* .
-- " F 1 . r
3 l I f I

-- _Ifl— —_

 

-21..

There was no relation between chick mortality and pullet mortality
when total mortality is considered. In fact, changes in pullet
mortality seem to be just opposite to changes in chick mortality.

Changes in chick mortality from leucosis complex are quite con-
sistent and downward and more related to changes in pullot mortality
than.when total mortality is considered. (Charts 1&8).

There seems to be a relationship between mortality from leucosis
complex and mortality from.other causes but the results are not always
consistent (Appendix, Table IIIa). From l93h to 1936, mortality from
leucosis complex decreased from.elevenp& three tenths percent to
three and three tenths percent and most of the other diseases de-
creased, yet mortality from the metabolic diseases increased.

From 1936 to 1937, leucosis complex and most of the other diseases
increased, while the metabolic diseases decreased.

When the birds are summarized by generations (Appendix, Table
IVc), the loss from leucosis complex decreases each year, while losses
from.other diseases show a decided increase in the second generation.

In 1938, in the group which includes all birds in families of
four and over (Appendix, Table IVb), total mortality'was twelve & five
percent, and in the third generation birds in families of four and over
(Appendix, TableIVd) it was nine & five tenths percent. The complete

list of causes of mortality in thesé two groups is given in Table 7.

 

i - ‘ ' ~1 141 Ch1 17 f' i

. T 1, Hom‘l’nht“ *Vom Leuco§ls comPle-x
«9+1- 1 H “”1": m. 34 defl
1%“03ftuh7‘r I 1 . , , p 1 ‘ ‘11

 

 

__—. _-.._4..._. ....

 

1

.-.--. .- ----.. , .,_..-_ __ . _l
f

!

...... [

,. ...- __ ._ .- -4

 

 

. .1, amalgam
1 11 . 1'11" I11 . 1T 1
' Arum-1531* 4-110917%. .

 

1

 

 

 

 

 

1.1. 11.. '1 I ,H ‘
195.4.“ 1 was; itwqa'é‘
4.-

1 . . . 1 . 1 3.1 V
v v. -- -7 . ..1.. - .. ..rf4v.. a... - .... .- -.H. ..1. .... .1 ......
1 1. . ~ e 3* = 1 . ,,. ~ 1.

. . , , .
I ' 9 | .

1 I
I x . .

I

 

 

 

 

 

 

 

 

 

 

  

 

 

 

   

 

 

 

: 111 :

g ..... i .. g 1i g 1. ;.
5....._1..._._........H--.-_....__l.-..._-....r.77...:1-_..._...1.--.-f-.__—~_p .. .-.--..-.-1-,.._....--.-....m ..r.-.-.-...--m....:|-._.._.aw....—_....an ’.- a .. -... “Hw1f11—r— -- -.___ ... ...
. ................. .. ; ._ ,. ‘ i .f- ,. £3 . o-
1:11;§' 11. ..' ' j “““ 1T8 1' 1_:.1 ‘
”11711711514111.11' ' 114117171 1 TN "'71; T11 1‘11 1.---,_, 1711,111rm—1wlc—bw 1”*"’ ”11'1'11'M‘;_' .. 11.1” 11 17411111111111. 4 ,1" ’ ' ‘ T11
a: " g .:f '.T ;,“.;.; MMGT‘tnhh‘ Wmlebtflpsr$na‘nfirieyrgg' 1
_i;,::'._. ..;. .::..,; :.. .;..; - ..... $4; in..- :..;.'.-..'-
293$ ~23. 1 “mks iii racesxiisaxgig ":1 ......

. . . .. ... ¢ . ...; W. .

is ““1. : ‘.. .. ..... .fi~ ~ ; tr -ww~-~wws

-.. vzmmamy 1: ..... '

.I.1....1.. L;1‘{ 1' i

:‘111:1§"31.1.3i-:.1 1, 1' ,
~— ,,,,,, .—----‘E-z:1+ 1 ~~~~~~ - - :

r g I
"11:711..“ "f“f‘" 111111111l1 ; .o .‘ . .4 . . . i .1 , . .

, . . : , 1~ 1 .i . Y 7 . _ ‘1, p .2 . V .
,1 -...-. _;-_a5l.-*_--.i.--_-.._ ' ' 1~~ --.. :. _.----” _ ._. ..----V..-i;---_..-._._ 1 _'_, __-..,.__---- L. _......;, --...-....
. c 1' _ 1 1 . ..., . .
I
-_ _-1..2..'_, - _.i.__
.. $ ‘ 4A
. . , . i .
g . --.z-.-._-. I.-- ‘ y_:_j__: r “ denesofiyraxerllli'- -.. ....--l..- _..... _ H
Tiff ' 7.;..I .; 1
.1”:;i-,1-"~--j1“ 3%‘f—F—Hddrgl‘ Q‘F‘H‘es- 1.“...13e‘oj1ed -— {S4311 #1:!4 7-1

 

111.;1 - f1 - ~ * :Gejaevn'ho‘ns '1 f."T‘.‘ '11

y..._._....__.-.. . n . 1. .. -« ——-.._....._.. ..‘..-A..--.... _.. . _.-fi. ....__ .___.__-__ . .. _.-.,.... .. v , . .-..--

..
. fi-___.. .. 4 . - . _-5

 

 

r. - ——-—.— ——7- ——1- -.——'_—-.o “no.-. ——--—-—— -

 

 

 

T-_-—-—_ r ‘,_. r ..‘—_- v
i o . I I
i

- Chnfl‘t 3
CovvclnTmn Cluck Mun-ta 1T! {Fund HoquUTY
1 Totq‘Hun-TnhTY All VGIYds.

.. * ""1

v
o
I——-—_ _..-—-I-.~1'l-

 

 

 

 

 

 

 

 

 

 

 

 

 

 

i
i. . :
, %?ol of. J 1 ,
5 M01- ql'uTy - * 1193.», i
' ' l
L--- -. .30 . - , -1
... . . 1
I .
1 1 15‘ ' ;. 1
r--- ~ M3» “ , ' ‘ , 1
gr” 1136 ‘ 1
'. .- 19 .. _Q .I
~ 193: I
.' ~ (’3 I
- 15'. _ .. mac 1
IL:".."1’ ' 0 T
. 6n. =: .133 ' 1
;. - - £0 1... A. ; l . e i 17 1
5 to 15' . 2.0 , 2.;-
% cm H: Mmmiry
1 a g :
l i I 1
_. . . f , . . 1 '
pn—.——— .-. -. ~.. ._ ...-. ..I - -— ..‘ ... ..: _..- _ ...“-.. _... . --.. ...--. '- _—- _ — —_ ...1 .... .. 0' -. — .— .4
'1, 1 1 . ; ' 'twraln‘hbn Civil; MQ+TQTITY11'PUUBTM+VTQTITY ;
1‘: " 1 1f“: ’1 ' 31:“ :1: 1 .. LeuwsisCuwanqy HUGH-aha ; "1 . 11 1 ’1' 1 1“
13.5w- :~~1%£ .. t j .1 . 1
: tint I - : . 1 '-. .. ~ . . .
.---.._--_..a. ..... V - —- *"T"‘1§‘SI¢”‘“+WT‘T * . : * -
In- .. i -.‘ - -- _
. . ._ '_ “"131 5
' G). 1
.. .- - -.1...,_.£-.--..-_.-.._....-- -- - - .. - - ---"--- - _ - - ._ -. -
1 1 i
1-_- : _
; (135‘ '
_ _ 6 ... EJ-
1138 ’
1.- ----.14.-- - Q. __ - 113.5 -_ _ - - 1
': . IL.- .511'6 .. Q
1-1.11 . 6).? ‘ 93.0,” . . . |
1 2 s , I L n . ,t
I 4- 5‘
r' . 11%1Cth—k [‘10deva
£11- .1- . _ Y- _ _ - - _
l1
!1 1 x .1
I' - 7 . f '
5 ;
4.1...1: -' ' . ~— «~ , 1:1 z 1 - . i1. .. L

n c---_-—- ... .1

 

Table 7

-22..

Causes of Mortality in Two Groups of Birds

with Low Total Mortality

Causes of
Mortality

Pickout
Salpingitis
Impacted oviduct
Enteritis

Liver diseases
Calibacillosis
Lymphomatosis
Leucosis
Laryngotracheitis
Impacted trachea
Obesity

Visceral gout
Peritonitis
Hemorrhage of heart
Unknown

Total died
% died

1938, All Birds
in families of
h and over

HHHwHHwaHNNHrN

b)
O

12.2

3rd. Generation
of Related lst,.
2nd,. & 3rd. Gen-
erations in ramp
ilies of h.& over

HHH HHrH H

\oti

.5

whenmortality‘is reduced to near ten.percent leucosis complex

still accounts for about one third of total mortality, reproductive,

digestive and metabolic diseases account for most of the balance

(Appendix, Table Vb and Vc).

There'was a small decrease in the survival age of the birds

vwhich died (Appendix, Table VI a to g) which is contrary to expectations.

-2 3..

It is true for all graups of diseases, even the leucosis complex. Gen-
erally, a reduction in the rate of mortality from leucosis complex is
accompanied by an increase in survival age.
The five year average survival age for diseases in the leucosis

complex group was:

Tumors 501 days

Lymphomatosis h26 days

Neurolymphomatosis 336 days

Leucosis 380 days

DISCUSSION

For inheritance studies, comparisons of characteristics by
consecutive years is not very accurate because pullets are trap-nested
a year before they are used for breeding and therefore have no progeny
until their second year. There should be more relation between alternate
years than between consecutive years. And even alternate years is not
a completely accurate comparison because some birds are used more than
once and may have progeny of more than one generation in the same year
(Appendix, Table 1).

Summaries by generations are also subject to error because some
birds of a particular generation may be produced in more than one year,
and there were no means at hand to measure variations in the amount and
virulence of plant infection from year to year.

The "t" tests to determine the significance of the comparisons are

shown in the following summaries:

Table 8

All Birds, by years

Consecutive Difference t value Alternate Difference
years in.% years in.%
19314.35 ‘6 o 1 lo 37 19311-36 '2 09
1935-36 3.2 .79 1935*37 lh.6
1937-38 -18.2 **h.55 193h-38 -9.7

All Birds in Families of four and over, by Tears
193h-35 -3.7 .73 l93h-36 -O.9
1935-36 2.8 .61; 1936-37 11.2
1936-37 8.h 1.85 1937-38 -7.5
1937-38 -15.9 “3.82 193h-38 -8.h

All Birds, by Generations

Generations Difference in % t value

lst & 2nd h.l l.h5

2nd.&.3rdx ~12.9 ‘**h.08

lSt 8: 3rd " 8.8 ”2072

All Birds in Families of four and over, by Generations

Generations Difference in % t value
181'. & 2nd 6.3 * 2.1
lst & 3rd - 7.3 *2.23

Related Generations, in Families of four’and over

lst &.2nd 11.6 1.72
and & 3rd '1508 *201113
lst & 3rd - h.2 .63

Related lst and 2nd Generations, in Families of h.& over

~2h-

t value

.73
“.13
*2005
*2058

.19
*2.28
*2.17

1.99

 

181': & 2nd 207 069
Related 2nd.&.3rd Generations, in Families of h.& over
2nd.& 3rd *'6.1 1.52
*signiflcant‘at’Sitlével

*8!- Qicfiif‘inant :1: 11 12:11:51

-25.

In general, the variations in total mortality are no greater than
would be expected for the number of birds inVolved. The comparisons of
alternate years are a little more consistent and a little more signifi-
cant than consecutive years but not enough so to justify and conclusions.
The value of the figures as a basis of eviden;e of genetic changes is
offset by'a high percent of mortality from cannibalism in the year 1937
(Appendix, Table IVa). Cannibalism is included in the reproductive
diseases, and in 1937, Was eight & four tenths percent higher than the av-
erage of the other four years. This also accounts for some, but not
all, of the high mortalityin the second generation birds.

The birds in the related lst., and 2nd., and 3rd. generations, in
families of four and over, ought to be the best measure of genetic
changes. The changes are significant, but the change from the let.
to the 2nd. generation is an increase of eleven.&.six tenths percent
while the change from the 2nd. to the 3rd. generation is a decrease of
fifteen.&.eight tenths percent ( Table 8). Some of this increase and
decrease is due to cannibalism in 1937, which year was largely second
generation birds. The value of the figures for this group is further
offset, hawever, by the small number of birds in the group. This group
represents birds in families of four and over which are descended from
hens in families of four and over, which are themselves descended from
first generation families of four and over. Only three third generation
families with only thirty one progeny are in this group (Appendix, Table
113).

Ther

 

decrease

flock. T
which is .
a positivi
hisdata w:
results a:

all chicks

 

The c
leucosis c
Significan
{Lions and
Tie cox-rel

The c
chicks and
“my.

Bears
of the m0]
md forty

01039 to 1

-26-

There is no explanation for the increase in chick mortality and the
decrease in mortality of pullets raised from the survivors of the same
flock. The correlation is, r = -.77 - .233 The "t" value is 2.266,
which is not significant for the five comparisons. Bryant (12), found
a positive correlation between chick mortality and pullet mortality when
hisdata was grouped by percent mortality in families. Just the opposite
results are obtained here when the data is arranged by years, including
all chicks and all pullets.

The correlation between chick mortality and pullet mortality from
leucosis complex is positive, r*- .56 - .SOh. The correlation is not
significant for the five comparisons. When the data is grouped by gener-
ations and includes all chicks and all pullets (Appendix, Table IIIc),
The correlation is, r = .9 - .09. This is a high degree of correlation.

The consistent reduction in mortality from leucosis complex in both
chicks and pullets is the most important and satisfactory result of this
study;

Bearse, et a1, (7) reported that leucosis complexcaused 30 percent
of the mortality in a resistant line during the first six years of breeding
and forty nine percent in a susceptible line. The thirty percent is
close to the results of this study after five years of selection. Other
investigators have noted that a reduction.in leucosis complex is
accompanied by a reduction in other diseases (11) (26) (bl). waters
(52) suggests that deaths from these two groups may have some association.
Is the reduction in other diseases due to the reduction in ne0p1asms,
or'vice versa? It may be that the presence of leucosis infection in.a

degree less than sufficient to cause death may predispose birds to other

infectio:
pr "uctiv
ality fr:

T48
increase
however,
W) days.
after 39'.
relative:

The
PeSistan;

'33 Surf:

-27-

infections. This view is supported by the fact that nonspecific re-
productive and digestive disorders still cause most deaths when mort-
ality from.neoplasms is reduced to allow percent by selective breeding.

The decrease in the survival age of the birds which died, when an
increase was expected, is difficult to explain. It should be pointed out,
however, that in the first year of the study (193h), the survival age was
hOO days. This is much higher than in most report of resistant strains
after several years of selection, and the variations from hOO days are
relatively'small.

The number of birds which die in a flock depends on the genetic
resistance of the birds and the amount of plant infection. That there
was sufficient infection in the environment of this flock is indicated
bythe mortality of the flocks of White Leghorns and Barred Plymouth Rocks
which were reared and housed with them. Both the Leghorns and the Rocks
had higher mortality, the Rocks being considerably higher. The method
of selecting breedng pens used for the Rhode Island Reds and described
in this paper, was not used for the Leghorns and Barred Rocks.

The mortality in this flock was reduced to a rate considerably below
the average for commercial flocks. It seems evident that part of this
reduction is due to genetic resistance developed by breeding from families
which had low mortality. Especially is this true for the reduction in
losses from leucosis complex. Part of the reduction may be due to reduced
infection, and the reduction in mortality fonn nonspecific infectionSImry

be coincidental with reduction in leucosis complex, but there is enough

evidence 0

eating the

 

hens are u
iii ten to
year the p

mh xfile e

-28-

evidence of increased genetic resistance to make it worth while to examine
whether the same method of selection used here could be used by commercial
poultrymen. The methods by which these birds were hatched, reared and
housed are similar to commercial farm methods. If the method of selection
could also be applied with the same results, the financial returns could
be greatly improved. The evidence is that it could be.

The method of selecting breeders which is the most accurate in esti —
mating their genetic make-up is the "progeny test" method. By this method,
hens are tentatively mated to adlale in individual pens, that is, one male
and ten to fifteen hens in each pen. 1'he chicks are raised and the next
year the pullets are trapnested and records of the progeny of each hen and
each male are compiled. On the basis of this records, the hens and nales
are"tested". The assumption is that the poultry man sould then proceed
to build a flock using these tested birds for breeders year after year.
The practical difficultyin the way of Such a procedure is that a hen or
a male would be three years old before it could be fully tested, and by
that time many would be dead and the rest would have relatively short use-
ful life left. It would also be necessary to carry many extra male bird 3
for three years until their families had been tested. It should also be
realized that the pullets which are being trapnested to prove certain hens,
males and families are an important part of the flock. A farmer could
never have an entire flock made up of tested or proven birds. Most of the

flock each year is being used to test or prove a few of the others.

tierested
ESiStanCE
9111? um
9-5 a mu.
331:“ this 3
between me;

Ti T327101-

-29..

A short cut to this method is the use of cockerels which are tested
on the basis of their sisters rather thn their progeny. This reduces
the number of males it is necessary to carry and permits their use at an
earlier age. Such a method was used in selecting males in this flock.
of the 26 different male birds used, only 3 were used twice. Most of them
were sib-tested cockerels used for the first time. Of the 190 hens used
for breeders during the five years, 1h3 were used only once, 3b were used
twice, and 13 were used three times.

'Ihe data offers an opportunity to examine another question which has
interested the writer for several years. The question is whether the
resistance which birds seem to develop against disease is a biological
entity which gives resistance ag ainst all diseases and can be transmitted
as a unit. Or is resistance developed against diseases one at a time and
only this limited resistance transmitted? waters (52) noted the relation
between mortality from leucosis complex and mortality from.other diseases,
and Taylor (h3) states that "individual families seem to vary greatly in
their ability to withstand particular diseases".

There is evidence here to support both sides. There are families
as large as 20 birds which had little or no mortality, sometimes fro more
than one year and when mated to different males. Hen No. N93h had 12
daughters in 1936 and no mortality; 1h daughters in 1937 and 3 died, one
each form impacted oviduct, cropbound and pickout; 8 daughters in 1938
and one died from laryngotracheitis; a record of 3b daughters in three

years and h deaths, none from leucosis complex. Hen No. N907 had 13

daughter
1 from ;
male an:
In 1936,
ters pr:
pingiti:

The
sis com;

high ~~

O‘olv"

-30.

daughters in 1937 and 7 died; 2 from leucosis, 1 from lymphomatosis,

1 from pickout, 3 undnown. In 1938, she had 6 daughters by'a different
male and none died. The best family in the five years was hen No. N583
In 1936, she had 2h daughters of which 2 died; in 1937, 7 of these daugh-
ters produced 60 pullets of which 5 died, 2 from leucosis, 2 from sal-
pingitis, and 1 from peritonitis.

'Ihere are instances of families which had high mortality from leuco-
sis complex and also other diseases, and others that had no neoplasms but
high mortality frOm other causes.

The term "vigor", is often used by poultry breeders and occurs con-
stantly in poultry literature yet it is a term that is hard to describe
and harder yet to measure. The cause of the present high mortality' in
poultry flocks is ofted blamed on the practice of selection for high pro-
duction'without accompanying selection for Vigor. Used in this way,
vigor, is synonymous with resistance to disease. This question is not
answered dafinitely by the data at hand but it is the considered Opinion
of the writer that there is no such thing as vigor, in the sense generally
used. It is not a biological entity. Vigor is a vague something which is

the result of good health, rather than the cause of good health.

CONCLUSIONS

A method of selection, using progeny tested hens and their families
mated to sib—tested cockerels, was effective in reducing the mortality

ina flock of Rhode Island Reds from twenty-three & two tenth percent

-31...

to thirteen.& five tenths percent and mortality from leucosis complex
from.eleven.& three tenths percent to four’& one ftenth percent. The
same method could be used by commercial farms. 8

When mortality'is reduced to thirteen percent, leucosis complex
causes about one-third of the total loss. Nonspecific reproductive,
digestive, and metabolic diseases cause most of the balance.

Reduction in mortality from leucosis complex diseases is accompanied
by a reduction in other diseases.

There is a relationship between the percent mortality from leucosis
complex in chicks and the percent mortality from leucosis complex in the
pullets raised from the survivors. The correlation for total mortality

between chicks and pullets is negative.

l.

2.

3.

h.

S.

6.

7.

8.

9.

10.

12.

BIBLIOGRAPHY

A study of poultry mortality, causes and preventative measures,
1936, The U. S. Egg and Poultry Magazine, XLII: h32-h3h.

Asmundson, V. 8., and J. Bieley, 1932, Inheritance of resistance
to fowl paralysis (Neurolymphomatosis gallinarum), Canadian
Journal of Research, VI: 171-176.

Barger, Edgar H., and L. E. Card, 1913, Diseases and Parasites of
Poultry, Philadelphia, Lea and Febiger, 3rd Edition.

Baton, William D. , Elementary Mathmematical Statistics, New
York, John Wiley and Sons, Inc.

Beach, Jr. R. , 1936, A discussion of poultry disease control, The
U. 3. Egg and Poultry Magazine, XLII: ho—hz.

 

, 1939, Importance of nonspecific pathological conditions in
causing mortality and culls in laying flocks, Cleveland, Pro-
ceedings Seventh World's Poultry Congress, 219-2hh.

Bearse, G. E. , D. F. McClary, and W. H. Miller, 1939, The results
of eight years selection for disease resistance and susceptibil-
ity in White Leghorns, Poultry Science, XVIII: hOO-hOl.

Biester, H. E. and L. DeVries, 19115, Diseases of Poultry, Ames, 1a.,
The Collegiate Press, Ind.

Bastian, C. H., and R. S. Dearstyne, 19%, The influence of breeding
on the livability of poultry, N. C. Agr. mp. Sta. , Tech. Bul.
79.

Brandley, C. A. , N. F. Waters, and W. J. Hall, 191:8, Fowl paralysis
and other forms of avian leucosis complex, Washington, D. 0.,
U. S. Dept. of Agr. Year Book, 91414-962.

Bryant, Reece L. , and E. P. Johnson, 191114; Incidence of mortality
in two strains of single comb White Leghorn chickens, Poultry
Science, XXII: 521-5211.

Bryant, Reece L. , 1915, A comparison of the mortality of single
comb White Leghorn growing pullets and laying hens, Poultry
Science, XXIV: h23-h25.

13.

17.

18.

19.

20.

21.

22.

23.

21;.

25.

Burmester, B. R. , 191:5, The incidence of lymphomatosis among male
and female chickens, Poultry Science, XXIV: h69-h72.

Burmester, B. R., C. 0. Prickett, and T. C. Blending, 19h6, The
occurance of neural and visceral lymphomatosis in chickens
proven immune to transplants of lymphoid tumor strains, Poultry
Science, XXV: 616-621.

Carpenter, Cliff D., and J. Holmes Martin, 1939: A gentic approach
to the control of adult mortality in the fowl, Poultry Science,
XVIII: 168-1714..

Darrah, L. B. , 19117, Make your poultry farm pay, Cornell Un. Exp.
Sta., Ext. Bul. 713.

Davis, Olive 5., L. P. Doyle, F. L. Walkey, and L. K. Canker,
191:8, Studies of avian leucosis, III. The incidence on avian
leucosis in various breeds of chickens, Poultry Science, XXVI:
h99-507.

DeOme, K. B., 19143, Intraperitioneal injection of lymphomatosis
nerve tissue into resistant or susceptible chickens, Poultry
Science, XXII: 381-391;.

Doyle, L. P. , 1928, Neuritis or‘paraylsis in chickens, Jour. Am. Vet.
Med. Assn. , LXXII: 585-587.

Gibbs, Charles S., 19311, Studies on neurolymphomatosis, Mass. Agr.
EXP. Sta., Bill. 308.

Gildow, E. H., J. K. William, and C. E. Lampmann, 19110, The
Transmission of resistance to fowl paralysis (lymphomatosis),
Idaho Agr. EXP. Sta., BT11. 235.

0038, L. J. , 1910, Classification of avian tumors, Cornell Veter-
inarian, XXX: 75-88.

Hartman, Roland C., and G. S. Vickers, 19146, Hatchery Management,
New York, Orange Judd Publishing Co.

Heisdorf, Arthur J. , N. N. Brewster, and J. H. Hooper, 191R, The
genetic relationship between mortality from induced and
spontaneous lymphomatosis, Poultry Science, XXVI: 67-73.

Hutt, F. B., J. H. Bruckner, and R. K. Cole, 1939, Reduction of
mortality in fowls by breeding, Cleveland, Proceedings
Seventh World's Poultry Congress, 149-51.

-31?

26. Hutt, 19h1, Four generations of fowls bred.for resistance to
ne0p1asms, Poultry Science, XX: 51h-526.

27. ---, 19h5, A test of fowls bred for resistance to lymphomatosis,
Poultry Science, XXIV: 56h-571.

280 Jeffrey, F. P., F. R. Beaudette, and Co Bo HUdSOD, l9h2, The role
of breeding in the control of fowl paralysis, N. J. Agr. Exp.
Sta., Bul. 696.

29. Johnson, E. P., 1932, A study in lymphomatosis in fowls (fowl
paralysis), Va. Agr. EXP. Sta., Tech. Bul. uh.

30. ----, 193b, The eitology and histogenesis of leukosis and
lymphomatosis of fowls, Va..Agr. Exp. Sta., Tech. Bul. 56.

31. Jull, Mbrley A., 19h0, Poultry Breeding, New York, John'Wiley and
sons, Inc.

32. Kennard, D. C., and V. D. Chamberlain, l93h, Pullet mortality,
Ohio Agr. EXP. Sta., Bimonthly Bul., XIX: 137-1h2.

33. Kissling, Robert B., 19h7, Leucoagglutination.as a serological
diagnosis of avian lymphomatosis, Poultry Science, XXVIz7h-77.

3h. Lambert, W. V., and.C. Wk Knox, 1932, Selection for resistance to
fowl 1yphoid in the chicken.with reference to its inheritance,
Iowa Agr. Exp. Sta., Res. Bul. 153, 261-295.

35. Lush, Jay L., Animal Breeding Plans, 19h5,.Ames, Iowa, The Col-
legiate Press, 3rd. Edition.

36. marble, D. R., 1939, Breeding poultry for livability, Pa. Agr.
Exp. Sta., Bul. 3770

37. Poultry disease investigations, 19h6, U. S. Regional Poultry
Disease Research Lab. , East Lansing, Michigan,.lfi.sc. Pub. 609,

38. Roberts, Elmer, and L. E. Card, 1926, The inheritance of resist-
ance to Bacillary'White Diarrhea, Poultry Science, VI: 18.

, 1935, Inheritance of resistance to bacterial infection
in animals, III. Agr. up. Sta., Bul. 1.19: 1.674193.

39.

 

ho. Segar, E. A., 1931, The pathology of fowl paralysis, with some
aspects of its cause and control, Veterinary Journal, LXXXIX:

h5h-h73.

hl. Sturkie, Paul D., 19h3, Five years of selection for viability in
White Leghorn chickens, Poultry Science, XXII: 155-160.

 

'i

hSo

h6.

h7.

h8.

1&9.

500

51.

52.

53-

She

55.

56.

57.

-35-

Taylor, Lewis W. , and I. M. Lerner, 1938, Breeding for egg
production, Cal. Agr. Exp. Sta., Bul. 626.

Taylor, Lewis W., I. M. Lerner, K. B. DeOme, and J..R. Beach, 19113,
Eight years of brogeny-test selection for resistance and sus-
ceptibility to lymphomatosis, Poultry Science, XXII: 339-31L7.

-----, 191111, An effect of ration on the mortality of laying hens,
Poultry Science, XXIII: 181-188.

Van Es. Leunis, and Jesse F. Olney, 19140, An inquiry into the
influence of environment on the incidence of poultry diseases,
Neb. Agro EXP. Sta., Res. Bul. 1180

, 19141, Poultry diseases and parasites, Neb. Agr. Sta. , Bul.
322, 1'90.

Waters, Nelson F. , 1911118, Close the flock to poultry diseases, U. S.
Egg and Poultry Magazine, L: 1115-1128.

--—-, 191411b, The hatcheryman's part in a closed flock system of
breeding, The U. 5. Egg and Poultry Magazine, L: 1453—1177.

-—---, 1914140, The breeder's part in a closed flock system of
breeding, The U. 3. Egg and Poultry Magazine, L: 500-503.

-----, 191:11d, The flock owner's part in a closed flock system of
breeding, The U. S. Egg and Poultry Magazine, L: 516-551.

Waters, Nelson F., 1915a, Natural transmission of avian-lymphomato-
sis, Poultry Science, XXIV: 226-233.

-—----, 1916b, Breeding for resistance and susceptibility to avian
lymphomatosis, Poultry Science, XXIV: 259-269.

----, 19115c, lymphomatosis in the chicken as influenced by
diallel crossing, Poultry Science, XXIV: 387-390.

----, l9b5d, Can the success of hybrids be duplicated.with
chickens?, The U. S. Egg and Poultry Magazine, LI: 100—1141.

 

, 191:7, Factors involved in mortality from avian lymphoma-
tosis, Poultry Science, XXVI: 639-6h7.

, and C. 0. Prickett, 191414, The development of families of
chickens free of lymphomatosis, Poultry Science, XXIII: 321-333.

 

Williams, J. K., C. E. Lapham, and G. C. Helm, 191:1, Low mortality
of station flock influenced by reduced virulence of infection,
Idaho Agr. EXP. Sta. h8tho Ann. Rpto, 239, 25-260

APPENDIX

-35-

ama am:
a»

:ma N4
om
we

How

unopmmsmo mnopmmsmo
nosmum nacho Ivonne

mnemonm

mum pm
pm
m
H
:m
HH
a»
mo
and
whopnmswn neopmwsmo
looses

koqowOMm new neon
nooee one no manaenqa
H canoe

OOH

0H

Om

NH

meopnmsmn

mesa

no

Ammav N
Aem.v H
Ammiv o
ism.v c
Acosv NH
Aam.v pa
Hm

Hmcflmwho

cannon

wmmH

wmma

pmma

mmaa

:mmfl

new»

Year

l93h
1935
1936
1937
1938

Number and Size of Families

Table IIa

By Years, All Birds

No. of Total
Families Progeny
51 18h
26 lho
b2 246
36 186
h2 267

Table IIb

Number and Size of Families

3.6
5.h
5.9
5.1
6.h

Ave. size
of Families

By Years, All Birds in.Fanilies of Four and Over

No. of
Tear Families
193k 21
1935 17
1936 26
1937 22
1938 32
Genel“ NO. Of
ation Families
1815. 92
2nd. 8?
3rd. 21

Number and size of Families

Total

Progeny

121
123
208
156
2&2

Ave.

Table IIc

size

of Families

5.8
7.2
8.3
7.0
7.6

By Generations, All Birds

Total
Progeny

378

h9o
15h

Ave. size
of Families

h.1
5.6
7.3

5 of the
Flock

65.8
88.0
81.h
8U.o
91.0

-38-

Table IId
Number and Size of Families
By Generations, All Birds in.Families of Four and Over

Gener— No. of Total Ave. size %.ofthe
ation Families Progeny of Families Flock
lst. hh 277 603 730k
2nd. 56 h26 7.6 87.0
3rd. 18 lb? 8.2 95.6

Table IIe

Number and Size of Families
Related lst. and 2nd. Generations, Families of Four and Over

Gener— No. of Total Ave. size
.ation Families Progeny of Families
lst. 22 153 6.9
2nd. hh 289 702
Table IIf

Number and Size of Families
Related 2nd. and 3rd. Generations, Families of Four and Over

Gener- No. of Total Ave. size
ation Families Progeny’ of Families
2nd. 13 126 907
3rd. 18 lb? 8.2

Table IIg

Number and size of Families
Related lst., 2nd., and 3rd. Generations

Gener— No. of Total Ave. size
ation Families progeny of Families
ISto 16 129 8.1

2nd. 33 25h 7.8

3rd. 3 31 10.3

a.: HH
p.w pa
m.m m
a.m m
m.HH Hm
none been
a .oz
mammdoooz

m.mH om
~.Hm mm
m.om om
H.sH em
N.mm me
cone come
a .oz
fleece

neceasa

new
one
new
one
red

powwow
.oz

s.a ea
H.: mm
m.m mm
s.~ ea
H.m mm
come some
a .oz
mammamooz

m.m~ oem ence
m.mH see new
m.aH are Free
w.mm ems mam
m.ea mmH one
cone cone
m .oz essence
Hence .oz

masses

ocean flea..nnnow am
nsmmHoooz Home hpafimpnos new hpfiawphoz Hence

wHHH manna

em
on
m:
an
Hm

Auuooooemv
meow .oz

mmma
amafl
emae
mmmfl
emae

meow

-hO-

~.m m
~.e NH
:.m N
c.m a
p.0H ma
none none
m .oz
nammfloooz

N.NH om
H.NN an
e.ma H:
a.eH HN
o.oN mN
echo echo
a .oz
Hence

nooaesa

oeN
omH
moN
aNH

HNH

powwow
.oz

m.H NH
m.H m
m.H ma
m.N as
m.N «a
been omen
m .oz
mammaoooz

o.NN Nee
N.m on
m.me mNH
o.sN mom
c.4H me
echo echo
a .oz
Hence

neoano

mmm
oom
Ham
mm:
me:

sarcasm
.oz

ho>o not 950m mo moflaflsoh_ofl mouam Add .mpmmM.hm

nsmmddooz Eon“ hpwameuoa new hpfiamvnoz Hopes
QHHH odnma

mm
mm
om
NH

Hm

Amnoooonmv
moom .oz

wmma
emma
pmma
mmmfl
amid

new»

m.n a
o.e 4N
m.m Nm
none been
a .oz
nsmmHmomz

OoHH NH
N.WN NHH
m.mH mp
Umflv Umflfi
& .oz
HMFOH.

mpmflddm

:mH m.H m m.NN oma mom
can ~.N om H.mH mmm momH
mum o.m Nm o.mH MNm waa

been been been omen
voodom m .02 R .02 oonoewm
.oz mammaaooz Hosea .oz

neoseo

cream Has .neoascnoaoe am
cansaeocz gone assaspnoe can assaspnoa Hence
oHHH canoe

Hm
um
mm

Amuoooonmv
moom .oz

.vam
.UCN

.enH

COHD.“
IIHOHHOU

 

A0>O HEW Hack HO meHflEdh CH Dvhfim HH< «WCOflpshbcow kW

nEnwdlooz EONH Rafiflauhofl 8:8 EJHHthOE HmuOh
UHHH 9H3 1H.

.hz-

e.m m

o.e HN

m.» HN
been moan
m .oz
mammadooz

m.m 2H Nee mm. m
H.mm OOH om: m.H om
m.ce we mmN m.N cN

none been soap moan

R .02 vomdom m .02
Hopes .oz mammamooz
upoHHdm

H.ma mOH cam
m.mH NMN Name
m.wa flea once
some some
n .oz coroner
Hence .oz

mxoflmu

nose can soon No nonsense as nonam Has .ocososnoace an

mammamooz Scum thHmvhoz one huflaspnoa Hmpoa
UHHH manna

HN
em
as

Amnoooonmv
mmom .oz

.osm
.oaN
.osa

scape
lacuna

e.m m

H.m :
ooflo been
a .oz
mammamooz

. 'ufllLlLSaIIITTI ,llllihlfillwi q~

m.m ea
o.mH 0N
cone rose
a .oz
Hence

mpoHHdm

NJH
me

oomsom
002

cm. m H.aH med
N.H a o.ea mm

some omen been some

m .02 & .oz
mammamooz ampoe

crease

04m
ma:

cognate
.oz

ma

Amuoooonmv
meow .oz

peso new poem Mo mofiafisom ma macepmnoooo .onm new comm oopnaom anneapmnooow hm
mammfioooz noun hpfiHmppos new headwpnom Hence

HHHH manna

.omm

moans
Inooow

Table IVa
Percent Mortality from Various Causes
By Years, All Birds

Cause 193h 1935 1936 1937 1938
Reproductive 3.8 2.8 2.h 11.3 2.6
Digestive 1.1 2.8 1.6 3.2 2.6
Leucosis Complex 11.3 5.7 3.3 8.6 h.1
Respiratory 101 007 102 201 lol
MbtabOliC 202 10h 609 201 105
Peritonitis & Nephritis 1.1 007 102 106 008
Miscellaneous 2.7 2.8 2.7 2.7 0.8
Totals 23.3 17.1 20.3 31.7 13.5

Table IVb
Percent Mortality from.Varous Causes
By Years, All Birds in Families of Four and Over

Cause 193h 1935 1936 1937 1938
Reproductive 5.8 3.2 2.9 10.3 2.8
DigeStive 000 302 10h 1.0 2.2
LGUCOSiS 10.7 507 30h 707 3.?
Respiratory 0.0 0.0 l.h 1.1 1.2
MbtabOlic 106 106 70h 1.9 106
Peritonitis & Nephritis 0.0 0.8 1.0 1.3 0.0
Miscellaneous 2.h 2.5 1.9 3.2 0.8
TOtalS 2006 1609 1907 28.1 1202

Table IVc
Percent Mortality'from.Various Causes
By Generations, All Birds
Cause First Second Third
- Generation Generation Generation

Reproductive 2.9 6.3 1.9
Digestive 1.6 3.1 1.3
Leucosis Compled 8.5 h.9 h.5
Respiratory 0.8 1.h 1.3
Metabolic 1.6 h.9 0,7
Peritonitis & Nephritis 1.1 1.0 0.9
Miscellaneous 3.h 2,2 0.7

TOtalS 1908 2309 1100

-h6-

Table IVd
Percent MOrtality from Various Causes
By Generations
All Birds in Families of Four or Over

Causes First Second Third
Generation Generation Generation
Reproductive 3.9 6.0 2.h
Digestive l.h 2.3 0.7
Leucosis Complex 7.h h.9 3.h
Respiratory' 0.0 1.6 1.h
Metabolic 1.7 5.1 007
Peritonitis & Nephritis 0.h 0.9 0.7
Miscellaneous 2.1 2.3 0.7
Tom]. 1608 2301 905
Table IVe

Percent Mortality from.Various Causes
By‘Generations
Related lst. and 2nd. Generations, Families of Four and Over

Cause First Second
Generation Generation
Reproductive 5.2 6.9
Digestive 2.6 2.8
Leucosis'complex 7.2 6.2
Respiratory 0.0 2.1
Metabolic 0.7 5.9 _
Peritonis &.Nephritis 0.7 0.7
Miscellaneous 2.0 3.8

Total 18.3 28.h

Table IVf

Percent Mortality from Various Causes
Related 2nd. and 3rd. Generations, Families of Four and Over

Cause Second
Generation
Reproductive 3.1
Digestive 0.8
Leucosis Complex 3.1
Respiratory 2.3
Metabolic 3.9
Peritonitis & Nephritis 1.6
Miscellaneous 0.8
Total 15.6
Table IVg
Percent Mortality from.Varous Causes
Related lst., 2nd., and 3rd. Generations, Families of
Four and Over
Cause First
Generation Generation

Reproductive 6.2 7.5
Digestive 0.8 2.0
Leucosis complex 6.2 7.1
Respiratory 0.0 2.0
Metabolic 2.3 6.3
Peritonitis & Nephritis 0.0 1.h
Miscellaneous 2.3 3.5
T3138]. 1708 2807

Second

Third
Generation

2.h
0.7
3.h
1.h
0.7
0.?
0.7

9.5

Third
Generation

0.0
3.2
3.2
3.2
0.0
0.0
3.2

12.0

-h8-

Table Va

ah9-

Causes of Mortality as a Percent of Total Mortality

By Years, All birds

Cause 1938 1935 1935 1937 1933
Reproduction 16.3 16.7 12.0 .f.25.0 19.h
Digestive h. 16.7 8.0 10.2 19.h
Leucosis complex h8. 38.2 16.0 27.1 30.6
Respiratory h.7 h,2 6.0 6.8 8.3
Metabolic 9.3 0.3 3h.0 .6.8 11.1
Peritonitis 8C Nephritis 14.7 ’402 600 5.1 506
Miscellaneous 11.6 16.7 18.0 8.5 5.6
Total 100.0 100.0 100.0 100.1 100.0
Table Vb
Causes of Mortality as a Percent of Total Mortality
By Years, All birds in families of four and over
Cause 1938 1935 1935 1937- 1938
Reprodective 28.0 19.0 11..6 36.1 23.2
Digestqfle 0.0 19.0 7.3 6.8 16.6
LGUC9318 complex 52.0 33.0 17.1 27.3 30.0
fieiptriFony 0.0 0.0 7.3 6.8 10.0
e a O 10 H 8.0 . O o .
Peritonitis & Nephritis 0.0 i.; 3i.g 2.2 13.8
“081131130“ 12.0 114.5 9.8 11.1; 6.7
TOtal 100.0 100.0 100.0 100.0 100.1
Table Vc
Causes of Mortality as a Percent of Total Mortality
Generations, All birds
Cause
First Second Third
Generation - Generation Generation
Reproductive
Digestive 13.3 $3.8 ‘ 17‘6
Leucosis complex ° - ’ 11'?
R . [T206 2005 bl.0
espiratory h.0 6 O 11 7
getimlt". . . 8.0 20.5 6.0
erltonitis & Nephrltls 5 8 h
Miscellaneous 17°3 9'3 5.;
Total . 100.3 100.0 99.8

'“rrs‘f

. um” i

 

.1

 

Causes of Mortality as a Percent of Total Mortality

Cause

Reproductive

Digestive

Leucosis complex
Respiratory

Metabolic

Peritonitis & Nephritis
Miscellaneous

Total

Table Vd

By Generations
All birds in families of four and over

First Second
Generation Generation
23.0 26.0

8.3 10.0
83.7 21.0
0.0 7.0
10.h 22.0
2.1 h.0
12.5 10.0
100.0 100.0
Table Ve

Causes of Mortality as a cause of Total Mortality
By Generations
Related lst. and 2nd. Generations, Families of four and over

Cause

Reproductive
Digestive
Leucosis
Respiratory
Metabolic

Peritonitis & Nephritis

Miscellaneous

Total

First
Generation

28.6
lh.3
39.h
0.0
3.6
3.6
10.7

99,9

Third
Generation

Zlch
703
3507
1h03
7.3
703
703

100.6

Second
Generation

2h.o
9.8
22.0
7.3
20.8
2.h
13.h

100.1

-51..

Table Vf
Causes of Mortality as a percent of Total Mortality
By Generations
Related 2nd. and 3rd. Generations, Families of four and over

Cause
First Second
Generation Generation
Reproductive 20.0 21.h
Digestive 5.0 7.1
Leucosis compled 20.0 35.6
Respiratory 15.0 1h.3
membOliC 25.0 7.].
Peritonis & Nephritis 10.0 7.1
Miscellaneous 5.0 7.1
Total 100.0 99.7

Table Vg
Causes of Mortality as a Percent of Total Mortality
Related lst., 2nd., and 3rd. Generations
Families of four and over

Cause First Second Third
Generation Generation Generation
Reproductive 3808 26.0 0.0
Digestive h.3 6.8 25.0
Leucosis complex 3ho8 2h.7 25.0
Respiratory 000 608 25.0
Metabolic 13-0 21.9 0.0
Peritonis & Nephritis 0.0 - 1.h 0.0
Miscellaneous 113.0 12.3 25.0

Total 100.1 99.9 100.0

.52-

Table VIa
Survival Age in Days
By Years, All birds

Cause 193A 1935 1936 1937
Reproductive 1106.1 1.129 293.6 393.1
Digestive 386 h30 h10.7 385.8
Leucosis complex 39h.7 h2h.1 3h2.7 37h.h
Respiratory 511 hh6 228 3hl.5
Metabolic 39h.5 393.5 267.9 883.5
Peritonitis & Nephritis 355.5 1198 321.6 1120.6
Miscellaneous h65.6 h51 h07.h 386.3
Average h00.1 h31.8 320.3 388.0

Table VIb
Survival.Age in.Days
By Years, All birds in Families of four and over

Cause 193h 1935 1935 1937
Reprdductive h06 h29 293.6 38h.2
Digestive h30 h39o3 379
Leucosis complex 387.h hhl.1 3h9.7 383.5
Respiratory 228 3hh
Metabolic 857.5 388.5 271 h27.3
Peritonitis 8: Nephritis 1498 327 1.169
Miscellaneous 1122.3 1133.5 386.2
Average h53.1 h36.7 332.5 387.7

Table VIc
Survival Age in Days
By'Generations, All birds
Cause First Second Third
Generation ‘Generation Generation

Reproductive hlh.h 36h.6 h38
Digesting h15.3 360.6 390.5
Leucosis h02.3 359.1 376.9
Respiratory h89.3 286.0 232.0
Metabolic 380.8 305.9 h6B.O
Peritonitis & Nephritis 367.5 383.2 532
Miscellaneous h77.7 h01.7 531
Average hl7.8 350.6 3950h

1938

385.1
318.7
388.1
250
369
h35.5
530

358.1

1938

371.h
295.2
388.1
260.3

h32o5
830
368.7

 

 

r «.113?!
.6 c

Table‘VId
Survival Age in Days
By Generations

All birds in Families of four and over

Cause

Reproductive

Digestive

Leucosis

Respiratory

Metabolic

Peritonitis & Nephritis
Miscellaneous

Average

First
Generation

hlh.5
280

h31.1
302.7
h98
tho

h18

Table VIe

Survival.Age in Days
By Generations
Related lst. and 2nd. Generations, Families of four and over

Cause

Reproductive

Digestive

Leucosis complex
Respiratory

Metabolic

Peritonitis & Nephritis
Miscellaneous

Average

Second Third
Generation Generation

353.6 h38
355.5 368
368.5 u12.6
286 232
300.6 163

398 532
hl9.5

3h8.9 h09

First Second
Generation Generation
hos 357.1
h61.7 3h5.8

hl7.5 37h
307.5
3th 303.1
h29 h69
39h h29.9
h15 358.5

 

 

JSLu-

Table VIf
Survival.Age in Days
By'Generations
Related 2nd. and 3rd. Generations, Families of four and over

Cause Second Third
Generation Generation

Reproductive h18.5 h38 f

Digestive 512 368 i

Leucosis complex 273 h10.6 3

Respiratory 258 232 ;

Metabolic 252.h M63 E

Peritonitis & Nephritis 327 3

Miscellaneous M61 531 E
E

Average 321.h h09 E___i,

Table VIg

Survival.Age in Days
Related lst., 2nd., and 3rd. Generations
Families of four and over

Cause First Second Third
Generation Generation Generation

Reproductive h06.7 363.h

Digestive 392 388.2 368
Leucosis complex h23.7 369.2 371
Respiratory 307.2 216
Metabolic 1402 306

Peritonitis &.Nephritis h26

Miscellaneous 531

Average hl9 360.3 371.5

Table VII

Diseases classified under various headings

Reproductive diseases

Pickout

Salpingitis
Internal eggs
Ruptured yolk
Hemorrhage of ovary
Cystic ovary
Impacted oviduct
Ruptured oviduct

Digestive diseases

Proventriculitis
Enteritis

Impacted crop
Impacted intestines
Inflammation of vent
Liver disease
Colibacillosis
Chronic coccidiosis

Leucosis complex

Tumors
Lymphomatosis
Neurolymphomatosis
Leucosis

Respiratory'diseases

Coryza
Laryngotracheitis
Impacted trachea
Roup

Metabolic diseases

Visceral gout
Obesity

Peritonitis and Nephritis

Peritonitis
Nephritis

Miscellaneous diseases

Parisites

Injury

Heat

Crippled
Hemorrhage of heart
Abscess

Unknown

!_ '-‘-'J‘hmu.-ljsliul" ‘ZC.

- .fll

 

 

 

 

) ‘ ..-; 80v! ('0‘. ‘ I. . . I. -..-(ll.
#8. ‘I o . ‘0.’ IO. .1! tk‘ulill‘.'ru '8.-. o, 7 o . D ...l in -‘o a .A. a 7 . n t. r.

 

14" .I‘!" #1 l4 . . I Ir 81"- I‘lli'n 3"I.-.

0
' VI 1. . \. ‘|‘ l-~ I b- al.‘ll I 0' 'l'- 1 All I 7 |-| \Il. 4’1
|’ 1‘ ‘