• TABLE OF CONTENTS
HIDE
 Front Cover
 Table of Contents
 Introduction
 Symptoms of crampy
 Literature cited
 Plan of investigation
 Results
 Discussion
 Summary and conclusions
 Acknowledgement
 Literature cited














Group Title: Bulletin - University of Florida. Agricultural Experiment Station ; no. 639
Title: Crampy
CITATION THUMBNAILS PAGE IMAGE ZOOMABLE
Full Citation
STANDARD VIEW MARC VIEW
Permanent Link: http://ufdc.ufl.edu/UF00027271/00001
 Material Information
Title: Crampy progressive posterior paralysis in mature cattle
Series Title: Bulletin University of Florida. Agricultural Experiment Station
Alternate Title: Progressive posterior paralysis (crampy) in mature cattle
Physical Description: 23 p. : ill. : ; 23 cm.
Language: English
Creator: Becker, R. B ( Raymond Brown ), 1892-1989
Wilcox, Charles J., 1930-
Pritchard, W. R
Publisher: University of Florida Agricultural Experiment Station
Place of Publication: Gainesville Fla
Publication Date: 1961
 Subjects
Subject: Paralysis, Spastic   ( lcsh )
Cattle -- Diseases   ( lcsh )
Cattle -- Diseases -- Genetic aspects   ( lcsh )
Genre: government publication (state, provincial, terriorial, dependent)   ( marcgt )
bibliography   ( marcgt )
non-fiction   ( marcgt )
 Notes
Statement of Responsibility: R.B. Becker, C.J. Wilcox and W.R. Pritchard.
General Note: Cover title.
General Note: Caption title: Progressive posterior paralysis (crampy) in mature cattle.
General Note: Bibliography: p.21-23.
Funding: Bulletin (University of Florida. Agricultural Experiment Station)
 Record Information
Bibliographic ID: UF00027271
Volume ID: VID00001
Source Institution: University of Florida
Rights Management: All rights reserved by the source institution and holding location.
Resource Identifier: aleph - 000927406
oclc - 18342696
notis - AEN8124

Table of Contents
    Front Cover
        Page 1
    Table of Contents
        Page 2
    Introduction
        Page 3
    Symptoms of crampy
        Page 3
    Literature cited
        Page 3
        Page 4
        Page 5
    Plan of investigation
        Page 6
        Page 7
    Results
        Page 8
        Page 9
        Page 10
        Page 11
        Page 12
        Page 13
        Page 14
        Page 15
    Discussion
        Page 16
        Page 17
        Page 18
        Page 19
    Summary and conclusions
        Page 20
    Acknowledgement
        Page 21
    Literature cited
        Page 21
        Page 22
        Page 23
Full Text



"CRAMPY"


a- I p


Progressive
Posterior Paralysis

In Mature Cattle
R. B. BECKER, C. J. WILCOX AND W. R. PRITCHARD

UNIVERSITY OF FLORIDA AGRICULTURAL EXPERIMENT STATIONS GAINESVILLE
Bulletin 639 J. R. BECKENBACH, DIRECTOR December, 1961
















CONTENTS
Page

INTRODUCTION ......-........------------------------ 3
SYMPTOMS OF CRAMPY ......... .- --------...----- 3
LITERATURE CITED ................----....- ------------------- ... 3
Congenital Paralysis in Red Danish Calves ..........------------------ 4
Congenital Paralysis in Norwegian and Polled Cattle ..........--.-.------ 4
Cerebellar Ataxia in Calves ........ ....----------.-------- 4
Familial Spastic Lameness of Calves .-...........------------- -- 5
Stringhalt of Cattle ........................ -- ....- -- 5
Neuro-muscular Spasticity or Crampy .--.-..-.....---- --.---.-..-.. 6
PLAN OF INVESTIGATIONS ......---------------------- .....-- 6
RESULTS ...............-........----.. .---- ..- ..- 8
Frequency of Occurrence ... ...-......------ ------ 8
Pedigree Study ................. ..... ..- ... .. --------- 9
Ayrshire ........... ....- .-.- ...-.-.-.. ---- ------------- 0
Brown Swiss ...........................---- ----- 10
Guernsey --......... ---------- -.- --- 10
Holstein-Friesian .....-........-.-----....------- 10
Jersey --- ----............--.----- --- -- --- 11
Holstein .............. ..........- -..--------- --- 11
Other Breeds ........-..........-.----- -- 12
STATISTICAL ANALYSIS ...........--.--...------. -- ------- 12
Frequency in Sire Groups and Lines -..- .........-.-------- ---------- 13
Chi-square Analysis ...................... ------....... -- --13
Distribution of the Gene(s) for Crampy in Dairy Cattle .......... ....... 14
A RECESSIVE CHARACTER ................-..... --------....-- .... .. 16
DISCUSSION ...-----...---------- ..------------- 16
Origin of Crampy -----.. ---......- ------------- 18
Practical Considerations .. ----.......... .......... -------- -- 18
SUMMARY AND CONCLUSIONS ... .................... ..-.------ 20
ACKNOWLEDGEMENTS ..----. ----------------- 21
LITERATURE CITED ........ --- -- .. .. ...... ---------------------- 21








Cover Photo-This 7-year-old bull became crampy as a 5-year-old. Note
his apparent desire to relieve weight from the left rear foot. The con-
dition was alleviated temporarily by periodic treatments.








PROGRESSIVE POSTERIOR PARALYSIS (CRAMPY)
IN MATURE CATTLE

R. B. BECKER, C. J. WILCOX AND W. R. PRITCHARD

INTRODUCTION
A physical condition known variously as crampy, paralysis,
progressive posterior paralysis, spastic syndrome, stretches or
Krampfigkeit has been recognized in cattle of both sexes for
years. It is characterized by intermittent spastic contractions
of the muscles of the back and rear legs of adult animals. The
cause of the syndrome has not been established, although a
familial pattern of occurrence has been reported. The condition
should not be confused with recessive calfhood ailments.
Crampy has shortened the useful lives of numerous bulls and
cows, and hence is of economic importance to the dairyman.

SYMPTOMS OF CRAMPY
Crampy occurs in otherwise normal, healthy adult cattle.
Symptoms become evident when animals are 3 or more years
old and usually are mild in the beginning. Earliest signs are
slight muscle spasms which occur when animals arise, back up
or move suddenly. As the condition progresses the muscles of
1 or both rear legs go into spastic contractions that last for a
few seconds to several minutes. Animals often extend or flex
their legs, 1 at a time, during these episodes. When both rear
legs are affected, they remain on the ground and are extended
backward during an episode, hence the term stretches. The con-
dition becomes progressively more severe over a period of months
or years until the muscles over the back, and eventually much
of the body, are involved. Because physical activity is necessary
to induce an attack, animals affected severely usually remain re-
cumbent. The value of animals is reduced as the syndrome
reaches advanced stages. They may become paralyzed com-
pletely in the rear quarters. Some deaths occur as a result in
advanced cases.
LITERATURE CITED
A recessive neuro-muscular condition has been recognized in
calves for some time both in America and in other countries.
It has been suspected that fetuses dying at 8 months and be-
coming mummies may be a manifestation of hereditary calfhood
conditions.








PROGRESSIVE POSTERIOR PARALYSIS (CRAMPY)
IN MATURE CATTLE

R. B. BECKER, C. J. WILCOX AND W. R. PRITCHARD

INTRODUCTION
A physical condition known variously as crampy, paralysis,
progressive posterior paralysis, spastic syndrome, stretches or
Krampfigkeit has been recognized in cattle of both sexes for
years. It is characterized by intermittent spastic contractions
of the muscles of the back and rear legs of adult animals. The
cause of the syndrome has not been established, although a
familial pattern of occurrence has been reported. The condition
should not be confused with recessive calfhood ailments.
Crampy has shortened the useful lives of numerous bulls and
cows, and hence is of economic importance to the dairyman.

SYMPTOMS OF CRAMPY
Crampy occurs in otherwise normal, healthy adult cattle.
Symptoms become evident when animals are 3 or more years
old and usually are mild in the beginning. Earliest signs are
slight muscle spasms which occur when animals arise, back up
or move suddenly. As the condition progresses the muscles of
1 or both rear legs go into spastic contractions that last for a
few seconds to several minutes. Animals often extend or flex
their legs, 1 at a time, during these episodes. When both rear
legs are affected, they remain on the ground and are extended
backward during an episode, hence the term stretches. The con-
dition becomes progressively more severe over a period of months
or years until the muscles over the back, and eventually much
of the body, are involved. Because physical activity is necessary
to induce an attack, animals affected severely usually remain re-
cumbent. The value of animals is reduced as the syndrome
reaches advanced stages. They may become paralyzed com-
pletely in the rear quarters. Some deaths occur as a result in
advanced cases.
LITERATURE CITED
A recessive neuro-muscular condition has been recognized in
calves for some time both in America and in other countries.
It has been suspected that fetuses dying at 8 months and be-
coming mummies may be a manifestation of hereditary calfhood
conditions.








PROGRESSIVE POSTERIOR PARALYSIS (CRAMPY)
IN MATURE CATTLE

R. B. BECKER, C. J. WILCOX AND W. R. PRITCHARD

INTRODUCTION
A physical condition known variously as crampy, paralysis,
progressive posterior paralysis, spastic syndrome, stretches or
Krampfigkeit has been recognized in cattle of both sexes for
years. It is characterized by intermittent spastic contractions
of the muscles of the back and rear legs of adult animals. The
cause of the syndrome has not been established, although a
familial pattern of occurrence has been reported. The condition
should not be confused with recessive calfhood ailments.
Crampy has shortened the useful lives of numerous bulls and
cows, and hence is of economic importance to the dairyman.

SYMPTOMS OF CRAMPY
Crampy occurs in otherwise normal, healthy adult cattle.
Symptoms become evident when animals are 3 or more years
old and usually are mild in the beginning. Earliest signs are
slight muscle spasms which occur when animals arise, back up
or move suddenly. As the condition progresses the muscles of
1 or both rear legs go into spastic contractions that last for a
few seconds to several minutes. Animals often extend or flex
their legs, 1 at a time, during these episodes. When both rear
legs are affected, they remain on the ground and are extended
backward during an episode, hence the term stretches. The con-
dition becomes progressively more severe over a period of months
or years until the muscles over the back, and eventually much
of the body, are involved. Because physical activity is necessary
to induce an attack, animals affected severely usually remain re-
cumbent. The value of animals is reduced as the syndrome
reaches advanced stages. They may become paralyzed com-
pletely in the rear quarters. Some deaths occur as a result in
advanced cases.
LITERATURE CITED
A recessive neuro-muscular condition has been recognized in
calves for some time both in America and in other countries.
It has been suspected that fetuses dying at 8 months and be-
coming mummies may be a manifestation of hereditary calfhood
conditions.







Florida Agricultural Experiment Stations


A review of the literature will help to distinguish calfhood
defects from those of mature animals.
Numerous genetic defects have been described in cattle (15,
16, 34).1 A number of them resemble in some respects neuro-
muscular spasticity or crampy. Although it is impossible to
classify all of the reported cases, most of them seem to fall into
6 spastic or neuro-muscular syndromes. Cases of idiopathic
lameness or contracture of tendons (8) or muscles (20) are not
included in this group.
Congenital Paralysis in Red Danish Calves (27, 30).-Calves
are born in a healthy state except for a posterior paralysis. They
are unable to rise on the rear legs at birth, gradually decline in
health, and die within a few weeks. No anatomical lesions have
been found, and the cause of paralysis is unknown. The syn-
drome is inherited as a recessive defect, tracing largely to 1 bull.
It has occurred in a rather high proportion (14 percent in 1948)
of the bulls in the Danish herd book (30). Since the condition
was recognized as hereditary, its appearance has been eliminated
largely through selection of sires, although many carriers may
remain.
Congenital Paralysis in Norwegian and Polled Cattle (39).-
A syndrome somewhat similar to paralysis in Red Danish cattle
has been described in Norwegian Red Polled cattle. This syn-
drome is characterized by flaccid paralysis of the muscles of the
rear quarters. Spasms of the forelegs and neck and corneal
opacities occurred in some of these calves. No lesions were found
in the central nervous system. It was attributed to an autosomal
recessive factor.
Cerebellar Ataxia in Calves.-A hereditary ataxia has been
described in Holstein-Friesian (1, 25), Hereford (21, 37), Ayr-
shire (23), Jersey (18, 34), Red Polled (40) and Shorthorn (31)
calves. Other similar cases in which histopathological examina-
tions of brains were not made have been reported. Possibly all
of these reports cover a single syndrome caused by varying
degrees of cerebellar hypoplasia and dysfunction.
The clinical symptoms of cerebellar ataxia vary markedly,
depending upon the extent of lesions in the cerebellum. The
most severe develops a characteristic decerebellar attitude with
orthotonus and opisthotonus, extension of the forelegs and flexion

1 Numbers in parentheses refer to Literature Cited in the back of this
Bulletin.







Progressive Posterior Paralysis in Mature Cattle


of the rear legs. Marked spastic contractions of the main muscle
masses occur when the animal is subjected to ordinary stimuli.
The contractions may occur in Otero, causing violent movements
of the abdominal wall of the dam. The most severely affected
calves die before birth or within 2 or 3 weeks after birth.
The majority of the cases of cerebellar ataxia in calves do
not exhibit the above marked clinical signs. Many appear nor-
mal at birth and may remain so for 6 to 8 months before symp-
toms appear. However, all of them develop some degree of
ataxia and most of them develop spastic muscle contractions.
Histopathological examination of the brains reveals varying
degrees of cerebellar defects.
innes et al. (21) reported a distinct familial pattern to cere-
bellar ataxia in Hereford calves. Saunders (34) studied 23
ataxic purebred Jersey calves and presented evidence that the
condition was hereditary in nature. He postulated an autosomal
recessive mode of inheritance. Turbes and Pritchard (40) also
noted that this syndrome was inherited as a recessive defect in
a herd of registered Red Polled cattle.
No clinical signs have been reported in carrier animals. Cere-
bellar ataxia also occurs in foals (19, 31), lambs (22), kittens
(12). puppies (9) and chickens (35).
Familial Spastic Lameness of Calves.-A familial spastic
lameness has been reported from Germany (17) and Great Britain
(13). Calves become lame in 1 or both rear legs between 1 and
8 months of age. The affected legs become straight, while the
head and tail are raised. Spastic contractions of the gastro-
cnemius and perforatus muscles occur. The condition progresses
rapidly, and within a few weeks the leg swings like a pendulum
and does not contact the ground. Walking becomes difficult,
and the animal must be slaughtered.
Stringhalt of Cattle.-A familial syndrome in cattle, resem-
bling stringhalt in horses in some respects, has been encountered
in Brahman cattle in Florida (33) and India. The earliest clini-
cal sign which becomes apparent is a sudden seemingly uncon-
trollable flexion of 1 or both rear legs which occurs when the
animal walks. As the disease progresses over months or years,
affected animals frequently drag their legs forward while ex-
tended as if the patella had immobilized the stifle joint.
A distinct sound often is made as the stifle joint is flexed.
Marked necrosis of the patella and distal end of the femur ensues.
Severely affected animals have difficulty in walking.







Florida Agricultural Experiment Stations


Neuro-muscular Spasticity or Crampy.-Neuro-muscular
spasticity (11) is a distinct clinical syndrome that occurs in ma-
ture cattle. The clinical signs of crampy summarized earlier can
be distinguished from the neuro-muscular syndromes described
previously in this publication.
Roberts (32) reported the syndrome in 33 bulls and 32 cows.
He cited 15 instances of both parent and offspring affected as
well as 2 full brothers, 2 half brothers, and a 3-generation group
of cows. Five breeds were involved. His evidence supported
that by Wirth and Diernhofer (42), who stated that the syndrome
affected cattle 6 to 10 years old and might be controlled by
genetic factors.
Frauchiger and Hofmann (14) found no histological lesions
in the brain. Roberts postulated that neuro-muscular spasticity
results from a derangement of the postural reflex mechanism.
La Fortune (26) of Quebec described a morbid spastic syn-
drome mainly in Holsteins. Woelffer (43) replied to a New York
inquiry about progressive posterior paralysis (crampiness) that
animals rarely were affected under 4 years old. The condition
responds to some treatments but recurs after temporary relief.
Two other experienced veterinarians (2) have had similar results
from treatment of crampy cattle.

PLAN OF INVESTIGATION
A study of useful tenure and reasons for disposal of bulls
from natural and artificial service has been under way for some
years (3, 4). Records were accumulated mainly by direct cor-
respondence with owners, managers and herdsmen having de-
sirable bulls in natural or artificial service. A direct question
as to the cause of crampiness, and the frequency with which
bulls were removed from service for "leg troubles," led to a re-
examination of records of bulls now dead. Records of groups of
closely related bulls were submitted to pedigree analysis through
3 to 5 generations, and familial relationships were established.
Reasons for disposal of these bulls were entered on the pedigrees,
as well as the ages at last effective natural service or semen
collection.
In this study not all cases of paralysis indicated on the records
were accepted per se as crampy because paralysis may result
from a number of different conditions. If described as a "stroke,"
it was presumed that the paralysis was caused by an embolism
or thrombus in the brain. Likewise, a crippling accident that







Progressive Posterior Paralysis in Mature Cattle


interfered suddenly with nervous control of a part of the body
was not considered as crampy. However, if paralysis developed
gradually in grown animals of either sex and involved the back
and rear quarters, it was considered to be crampy.
A list of reasons reported by the owners as causes of removal
from service includes: back and hind legs gave out,* became
crippled in hind quarters and couldn't mount, crampy and unable
to mount,* creeping paralysis of hind legs,* hind quarters failed
him,* lost use of hind legs,* muscle spasms and crampy,* muscu-
lar spasms,* neuromuscular spasticity,* polyarthritis,* progres-
sive arthritis,* progressive posterior motor paralysis,* progres-
sive posterior paralysis,* spasticity,* spastic syndrome,* unable
to stand up on hind legs,* unable to mount. Advancing age was
not considered as crampy even though some bulls were eliminated
for "age" as young as 7 years old. Hence it is believed that
records considered as crampy are on the conservative side.
The completed records of bulls over 312 years old were tallied
to estimate distribution of affected animals within the breeds.
Calculations were made of the standard deviation of ages at
last service, and distribution of the gene for crampy under ran-
dom matings. The chi-square test (38) was applied to the
frequency of occurrence in Guernsey and Holstein-Friesian bulls
when the record files contained the completed records of 4 or
more sons of individual sires.
Animals were considered crampy if the reason for disposal
as given by the owners was listed as crampy or a synonym. Some
diagnoses of rheumatism and gradual loss of use of the hind
legs were accepted in estimating frequencies if closely related
animals were definitely crampy. Other conditions which may
have been crampy but which were excluded were: age, unable
to mount, and refusal to serve. Paralysis alone was not con-
sidered crampy, as explained earlier. Estimates of the frequency
of crampy thus doubtless would be somewhat conservative.
The literature (7, 10, 36, 41) was searched as to the channels
whereby the gene could have spread among the breeds of cattle
under investigation.

Descriptions indicated with an asterisk were believed to be crampy,
while those not marked were regarded as questionable or from other causes,
and hence records of such bulls were disregarded.







Florida Agricultural Experi:nent Stations


RESULTS

FREQUENCY OF OCCURRENCE
Search of the completed records of bulls past 31/3 years old
for which reasons of disposal from service were at hand resulted
in 12,387 records of dairy and 448 beef bulls. The tally of bulls
removed or that died of crampy (under its several synonyms)
totalled 323 dairy and 10 beef bulls of 9 breeds. The dairy bulls
were removed from service at an average age of 10.02 years,
with a standard deviation of 2.49 years. They ranged between
3 and 16 years old at the last effective service or semen collection.
The spastic syndrome develops gradually and may not be recog-
nized in the early stages. Some of these spastic bulls had been
retained as long as usable despite the condition, because of their
ability to transmit factors for desirable production to their
daughters.
Records of the dairy bulls had been obtained from most
Canadian provinces and from every state except Hawaii and
Alaska. Crampy bulls comprised 2.6 percent of this population.
Among the 5 dairy breeds, frequency ranged from 1.9 to 3.9
percent. Chi-square analyses showed that frequency of occur-
rence differed significantly (P < 0.01) among breeds. The ages
at which crampy dairy bulls were removed from service are
shown in Table 1.
It may not be justifiable to emphasize breed prevalence of the
condition because of the limited number of records at hand of
some breeds. Other animals may have had the condition, yet
the owner regarded another cause as more prominent in stating
the reason for disposal. Or he may have reported "age" as the
reason for disposal when the bull was only 7 years old, in which
case the record was not tallied among crampy animals.
Muscular spasticity or crampy was indicated as the reason
for disposal of 18 bulls of 6 breeds before they were 6 years old.
See Table 1. Twenty-two others were discarded as 6 year olds
for this reason. Owners sometimes retained crampy bulls that
transmitted good production, even though they might be unable
to mount and semen had to be collected with an electro-ejaculator.
The condition advanced to the final stages when some bulls could
not rise to their feet. Sixty-five of these bulls died of the con-
dition.








Progressive Posterior Paralysis in Mature Cattle 9

TABLE 1.-AGE AT DEATH OR DISPOSAL OF CRAMPY DAIRY BULLS.
Age I I
in Ayrshire Brown Guern- Holstein- Jersey Total
Years Swiss j sey r Friesian
Total number removed

1 232 803 3,166 4,145 3,041 12,387

Number removed for crampy

3 ............ 1 .. 1
4 ....... .. 1 1 4 1 7
5 ........ 2 .... 5 1 8
6 2 1 2 11 4 20
7 5 1 6 17 3 32
8 .4 .... 8 16 1 29
9.... 5 3 9 27 11 55
10 .. 10 3 10 22 10 55
11 ....... 9 2 10 17 9 47
12 ... 4 4 8 15 8 39
13 ..... 3 1 3 5 2 14
14 ........ 1 2 2 2 7
15 ...... 1 1 2 .... 4
16 ........ 2 1 .... 3 i .. 5


Total 48 16 60 147 52 323

Percentage 3.9 2.0 1.9 3.5 1.7 2.6


PEDIGREE STUDY
Records of bulls of the dairy breeds were used in the study
of pedigrees of affected and unaffected animals within family
groups. Evidence of the hereditary character is based on the
frequency of occurrence among family groups. Some of the
related individuals were in widely separated parts of the country,
in herds under excellent management. From 1 to more than 8
sons of certain sires were affected, whereas other sons of the
same sires showed no outward symptoms of the condition. A
number of cows had 2 affected sons, some in separate herds.
Ayrshire.-One Ayrshire bull died when 9 years old of a
blood vessel rupture at time of service. Seven sons were 7 to
past 15 years old at death or disposal for crampy. One of them
was inbred. Another crampy son was out of the sire's paternal
sister. Six of the 7 crampy sons traced through their dams to a
particular bull in the first, second or third generation. Other
affected descendants included 4 grandsons, a great grandson, a







Florida Agricultural Experiment Stations


double great grandson, a triple great grandson and 5 great great
grandsons. Some 22 sons of this bull were not crampy at disposal.
Another Ayrshire bull had a crampy son. A crampy grand-
son had a crampy son in turn. The latter had a maternal brother
affected likewise.
Brown Swiss.-The 16 Brown Swiss reported with progres-
sive posterior paralysis or a condition described similarly as
affecting the hind quarters had the following pedigree relation-
ships: 2 paternal brothers; 2 sired by full brothers; a bull and
his son affected; a bull and his grandson affected; and 1 bull
with 3 great grandsons all affected similarly.
Guernsey.-A bull left service at 10.6 years because of "in-
jury to the stifle," while his sire was removed at 9.1 years for
"stiff hind legs." Three sons of the first bull went out at 10.95
to 14.9 years for "acute rheumatism," a "twisted stifle," or
partial posterior paralysis. A grandson lost use of his rear legs
at 12.3 years; another was slaughtered at 10.9 years for "back
injury"; and a third at 11.3 years for posterior paralysis. Two
great grandsons, themselves three-quarter brothers, were slaugh-
tered or died of posterior paralysis at 7.2 and 11.6 years of age.
Nine other descendants tracing more distantly 1 to 4 times to
the original bull were slaughtered at 7.7 to 11.1 years old for
crampiness or extreme crampiness. There were 4 successive
generations of crampiness in bulls of this family.
In two instances, a bull, his grandsire and 2 great grandsires
were crampy, as was also a double great grandsire-4 gener-
ations in the male lines. These animals were removed from
service when 6.3 to 13.5 years old.
One bull, his sire, double grandsire and double great grand-
sire were all affected.
Holstein-Friesian.-Eight sons and 9 grandsons of a popular
Holstein bull were crampy at death or disposal. One popular
Holstein bull was disposed of for catarrhal enteritis at 10.6
years of age. Eight of his sons and 14 grandsons were crampy
at death or disposal. Two of these affected sons were full broth-
ers. The affliction apparently is not transmitted as a dominant
character, as other sons and grandsons went out of service for
other reasons at 5 years old on to advanced age. The character
skipped generations in being manifest.
Another outstanding bull lost the use of his rear leg when
10.3 years old. Crampy descendants included a son, 2 grandsons







Progressive Posterior Paralysis in Mature Cattle


and 4 great grandsons, 2 of which were full brothers and 2 were
three-quarter brothers.
Both grandsires of a bull removed for "rheumatism in the
hind legs" at 8.6 years old went out because of paralysis in the
rear quarters or for "rheumatism."
One Holstein bull was removed because of age at 14.7 years.
His sire had been removed because of "injury to hind leg" when
14 years old. The bull served in a large herd where apparently
few mates carried the factors) for crampy. Of many progeny,
a son had posterior paralysis, as well as 2 grandsons and 3 great
grandsons. Two of the latter were fifteen-sixteenths brothers.
Many other bulls which descended from this animal were disposed
of for other natural causes. This family supplied further evi-
dence that the gene or genes for crampy apparently were not
dominant.
One bull, his sire and both grandsires went out of use because
of the spastic condition, failure of the hind quarters, or paralysis
-according to statements by the respective owners. Two full
brothers in this family were affected.
A bull, his son and several of their daughters were reported
crampy in an institutional dairy herd.
A group of crampy Holsteins included a cow, her 2 sons and
a grandson. Her mates were closely related bulls; one died of
unknown cause when 3 years old, and the other was reported to
have "an injured leg" at 11.8 years.
Jersey.-Pedigree study found the following family relation-
ships among 52 Jersey bulls reported with progressive posterior
paralysis affecting the back and rear quarters. One bull with
posterior paralysis had the following descendants affected: 3
sons, 2 grandsons, 6 great grandsons. One of the great grandsons
was a double great grandson. A living great grandson also is
crampy. Three of the great grandsons that died in widely
separated parts of the country with paralysis of the back and
rear quarters and the living crampy great grandson were all
three-quarter brothers.
A sire and son both were affected. A third sire had a grand-
son and a great grandson also affected. A fourth bull in a well
managed herd went out for "mineral deficiency." His grandson
and 2 great grandsons were disposed of at 6 to 12 years old with
rear quarters affected.
Holstein.-A Holstein cow, born in the Florida station dairy
herd, was 5 years old when clearly recognized as crampy. She








Florida Agricultural Experiment Stations


assumes a stance with hind legs as far back as possible, to bear
much of her weight on the forelegs. During an attack of the
spastic syndrome, she extends the right rear leg backward and
laterally. A picture of this cow during 1 phase of such an episode
is shown in Figure 1.


Figure 1. Typical spastic symptoms of progressive posterior paralysis
or crampy were recognized in this Holstein cow (H-21) first as a 5-year-old.
Note the stance of her right rear leg during an episode.

Other Breeds.-Of 251 Milking Shorthorn bulls, crampy in-
dividuals included 1 each at 6, 8 and 9 years old. One crampy
Angus bull out of 91 animals was removed at 10 years old. A
6-year and an 11-year-old beef Shorthorn were eliminated among
the 32 animals. Two Herefords were crampy at 3 years old, and
1 each at 8 and 9 years, among 74 animals. This was 2.2 per-
cent of the 448 beef and dual purpose animals.

STATISTICAL ANALYSIS
Since large numbers of Guernsey and Holstein records were
available, pedigree and statistical analyses were made of their
records. Fewer groups of Ayrshire, Brown Swiss and Jersey








Progressive Posterior Paralysis in Mature Cattle


bulls that included 4 half-brothers were available from the pedi-
gree study, hence were not used in this statistical analysis.
Frequency in Sire Groups and Lines.-Pedigree study enabled
the grouping of normal and affected bulls into sire groups (pa-
ternal half-sibs to full-sibs). Where closely related bulls oc-
curred, they were grouped into lines. Where the members of a
line were crossed with unrelated females, the sons were desig-
nated as a line-cross. The requirement was added that a sire
group, or a line or line-cross, must have consisted of at least 4
individuals. Only Guernsey and Holstein bulls past 5 years old
were included in the chi-square analysis.
Chi-square Analysis.-Records of 366 males representing 47
sire groups and 492 males of 42 lines and line-crosses were
utilized. It was assumed that if crampy were due to non-genetic
factors, it would occur in these categories in a random fashion.
Chi-square analysis showed that this hypothesis was rejected
at the 4 and 1 percent levels, respectively, as shown in Table 2.

TABLE 2.-FREQUENCY AND DISTRIBUTION OF CRAMPY SONS AMONG SIRE-
GROUPS AND AMONG LINES AND LINE-CROSSES.
Total J Number ]
Breed Number of Crampy Degrees of Chi-square
of Sons* Sons Freedom
Among Sire-groups

Holstein .........-- 183 26 20 26.9
Guernsey ......... 183 10 25 36.0
Combined ...... 366 36 45 62.9**

Among Lines and Line-crosses

Holstein ........- 235 35 18 33.1
Guernsey .... 257 17 22 33.8
Combined ........ 492 52 40 66.9t

*In groups of 4 sons or more.
** P < 0.04
t P < 0.01
Other than the affected animals mentioned previously, additional
groups were relatively free of the condition. Among sire groups
the following extremes in occurrence of crampy were noted: 0
affected among 18 sons and 0 of 19 sons. These were opposed to







Florida Agricultural Experiment Stations


2 crampy out of 4 sons, 6 of 23 and 7 of 23 sons. Among the
line and line-cross groups, there 0 crampy among 19 sons, 1 to
23 and 1 of 61 sons. Other line and line-cross groups, in contrast,
had 6 cases of 23, and 12 of 53 sons.
One might assume that the observed distribution could have
been caused environmentally under certain circumstances. Sires
under a common management in a given climate could have
tended to leave the herd for similar reasons. However, diagnosed
cases of crampy represented many herds and studs, and cases
were reported in different years. Group members rarely were
located centrally. Under these conditions the presence of genetic
factors was indicated strongly by the analysis.

DISTRIBUTION OF THE GENE(S) FOR CRAMPY IN DAIRY CATTLE
Crampy bulls were found in the records of the 5 dairy breeds.
The 12,387 records of dairy bulls were analyzed to estimate the
distribution of the postulated recessive gene for spasticity, as-
suming the character to be inherited as a simple recessive. The
formula for gene frequency in the make-up of the germ plasm
is the following, according to Lush (28):
q2 + [2q x (1-q)] + (1-q)2 1.00
Let (1- q)2 equal the distribution of actual crampy bulls,
which was 323 divided by 12,387, or 2.6076 percent. (1 q) then
equals 0.1615. Therefore q equals 1.00 0.1615, or 83.85 percent
of the population.
Substituting values in the formula -
(0.8385)2 + [2 q x (1 q)] + 0.0261 = 1.00
0.7031 + 0.2708 + 0.0261 = 1.00
(free) (carriers) (crampy)
Interpretation of the calculation is that for each 2.6 percent
of crampy bulls in the population under random mating prac-
tices, there would be 27.1 percent of heterozygous carriers not
showing spasticity but which may transmit the gene to one-half
of their offspring. Some 70.3 percent of the cattle population
should be free from the conditioning gene. Since they were not
carriers their first generation progeny would not develop the
symptoms at any time between 3.5 years and advanced age, if
they survived to a natural life span.
Since all these dairy animals were purebred bulls and repre-
sented male seed stock used, a similar wide distribution could be
expected in commercial cattle.
























H-21
Born Oct. 7, 1955
Photo Oct. 21, 1960
(See Figure 1, page 12)
Crampy in both rear legs


Sire................
a carrier


Girandsire








Granddani


D am ............. .........
a carrier

Slaughtered at 6.(i yrs.
as a non-breeder


Grandsire_








Granddam.


Figure 2. Pedigree of a crampy cow in the Florida station dairy herd. A carrier is the
animal.


Great grandsire
a carrier



Great granddam
may be a carrier


Great grandsire
a carrier



Great granddam
may be free


Great grandsire
a carrier



Great granddam
may be a carrier


Great grandsire
may be a carrier



Great granddam
may be a carrier

progeny, or parent, of a crampy







Florida Agricultural Experiment Stations


Occurrence of the condition in older cattle and freedom from
the condition in many individuals of afflicted families could be
ascribed to incomplete penetrance, if the character was truly in-
herited as a simple autosomal recessive. The condition would
not be evidenced in heterozygous (carrier) animals, but would
develop frequently when the animals had acquired the gene from
both parents homozygouss) and had reached 3 years or older.

A RECESSIVE CHARACTER
A known carrier of a recessive gene is either the parent or
the offspring of a crampy animal.
If crampy were inherited as a simple autosomal recessive,
both the sire and dam of the Holstein cow in Figure 2 must have
contributed the recessive gene for crampy in order for this cow
to develop the condition at maturity. Her dam was slaughtered
at 6.6 years old as a non-breeder and never exhibited the spastic
condition. Exact evidence is lacking on the grandparent genera-
tion as to which animals were heterozygous; all 4 could have been
carriers. Among the great grandparents, 3 bulls were suspected
as being heterozygous (carriers). One other bull and 3 cows in
this generation were possible carriers, as each of them had at
least 1 crampy grandparent. The pedigree of this crampy cow
in the Florida station dairy herd is shown in Figure 2.

DISCUSSION
Observations of different owners are reflected in the names-
such as progressive posterior paralysis-that have been applied
to the progressive spastic condition which sometimes affects the
back and rear quarters of some cattle 3 years old or older. The
condition is not related to the calfhood conditions mentioned in
the literature as affecting these parts of the body.
Evidence of genetic influence on crampy appears conclusive.
Frequencies of the condition occurring in the 5 dairy breeds, a
dual-purpose and 3 beef breeds differed significantly. Crampy
occurred in cattle within some closely-bred family lines and did
not occur in other equally closely-bred but unrelated lines. The
character developed in animals where both the sire and dam were
affected. Some full brothers were affected, as well as other
closely related animals. A crampy cow in a well-managed herd
had 2 crampy sons. Several other cows dropped 2 crampy sons
each, some of the pairs' being full brothers. The fact that 3
three-quarter brothers died of the condition in different years







Progressive Posterior Paralysis in Mature Cattle


in distant locations and a fourth is affected now tends to exclude
environment as the causative agent. However, environment may
have contributed to the intensity of the symptoms after they had
developed. All of these observations indicate that the condition
is hereditary.
The character is neither sex-linked nor sex-limited. It oc-
curs in bulls and cows, as well as in some first generation progeny
of affected animals of either sex. Exhibition of the condition
sometimes skipped a generation, as in an animal and its grand-
sire, hence it does not act as a dominant character.
Possibly the exact mode of inheritance may never be learned.
It is not impossible that multiple gene inheritance could be in-
volved, with the condition inherited in the manner of some quan-
titative characters. There are numerous instances from pedi-
gree analysis, however, that followed the pattern typical of re-
cessive red hair coat in Holsteins (6). The condition is appar-
ently not evident in heterozygous condition but is manifest in
homozygous condition with mature animals, hence has incom-
plete penetrance.
If crampy is inherited as a simple recessive, as suggested
from these records and analyses, then its gene frequency would
be about 16.2 percent. Of this proportion 2.6 percent of the
genotype would be the homozygous recessive (crampy), 27.1
percent heterozygous (carriers) and 70.3 percent homozygous
dominant or free from the gene.
Incomplete penetrance would necessarily make this estimate
of gene frequency low, since many animals doubtless left the
herds before the condition was recognized in them, and thus
they were assumed free. These suppositions do not preclude the
possibility that polygenic inheritance may be involved.
The average disposal age of the 333 crampy bulls (10.02
years) was higher than the over-all age of disposal of desirable
bulls from artificial service (3, 4). Some affected animals were
discarded under 4 years old. and some bulls transmitting high
milk production would have been retained longer, had it been
possible.
ORIGIN OF CRAMPY
Where did the gene for crampy originate? Since the herd-
books of the 5 dairy, 1 dual-purpose and 3 beef breeds have been
"closed" in America, it could not have spread between breeds in
the western hemisphere. These breeds developed in the British
Isles, (C i!i... Islands, the Netherlands and Switzerland. Also,
the name Krampfigkeit is German. Such wide intermingling







Florida Agricultural Experiment Stations


could have occurred through the transfer of cattle between some
of the nobility in the feudal period, before improved breeds were
recognized as such. Wide distribution within some breeds has
occurred in America because of popularity of prominent families
that happened to carry the recessive gene, then unrecognized
as such.
Evidence may be drawn from the movements of people with
their cattle among regions. Wilson (41) concluded that the dun
coat color, as well as the polled character, was distributed with
cattle taken by the Norsemen to their settlements across the
North Sea in the British Isles, Channel Islands and France be-
fore the feudal period. That source of the polled character traces
to Bos akeratos Arenander, a polled species in Scandinavia.
Duerst (10) concluded that the large size of the Rigi race (largest
strain of early cattle in central Switzerland) developed in the
district where German immigrants brought some of their cattle
in the feudal period. These cattle were a cross bearing the blood
of Bos longifrons Owen and Bos primigenius Bojanus. These
were the small domesticated cattle brought in the migrations of
Neolithic man to Europe, and the great wild ox of Europe. Herds
of cattle in the Netherlands were reduced by epidemics, floods
and wars and were replenished in part from surrounding areas.
Some foundation animals of the Shorthorn breed ("Dutch"
cattle) came from the Netherlands to the northeast coast of Eng-
land when Dutch engineers helped to drain the coastal fenlands
and later in illegal importations (7, 36). Some of this stock from
Durham was in the foundation of Ayrshires in southwestern Scot-
land. These early movements of foundation cattle are sufficient
to explain also the spread of hereditary characters from north-
western Europe to the breeds in this study. Such movements
occurred mainly before improvement of breeds in those countries,
and antedated Johann Gregor Mendel's discovery (29) of the
principles of hereditary by 1 or more centuries.
The gene (s) for crampy could also have arisen spontaneously
in each breed, although it seems doubtful that mutations for
crampy would have occurred in all breeds. This could have been
the case if the gene were unstable and thus more easily subject
to mutation. Either explanation is conjectural, although the
first one seems the more probable.
PRACTICAL CONSIDERATIONS
When the condition crampy is observed in an animal in a herd,
what action should be taken by the owner?







Progressive Posterior Paralysis in Mature Cattle


In the past, some crampy bulls and cows transmitting some
desirable characters have been used as breeders in the advanced
stages, being treated with pain-relieving drugs (44) or under
heat lamps to alleviate the condition individually. Such treat-
ment has a physical effect but does not change the germ plasm.
Some crampy bulls have been collected with electro-ejaculators
when unable to mount. These bulls have been esteemed because
of some desirable traits which they possessed. The popularity
of their respective progeny indicated regard for ability to trans-
mit producing ability. The crampy condition is distributed wide-
ly enough and is of sufficient importance in shortening the use-
ful lives of dairy animals that some consideration should be given
when breeding to known affected bulls or raising heifers from
crampy cows. Breeders may wish to consider crampy when se-
lecting future herd sires, should their ancestry be known as car-
riers.
Since the crampy condition may well be conditioned by a sin-
gle recessive gene, and is not manifest in heterozygous condi-
tion, there may be instances when a breeder might use a bull
for other of his desirable qualities. A carrier bull would con-
tribute the undesirable gene to 1/2 of his progeny on the average,
and not to the other 1/2. It would not be desirable, however, to
follow such a bull with another known carrier, or to mate a
crampy cow to a crampy or carrier bull.
A crampy bull would contribute the gene(s) to all his progeny,
but the condition would not manifest itself in the first-genera-
tion offspring, if none of his mates were carriers. A crampy
bull mated to a crampy cow may be expected to produce only off-
spring that would be predisposed to develop the condition in time.
If an animal develops the crampy condition, the owner needs
to analyze his whole herd. If a parent was crampy, all first-
generation offspring would be carriers, hence all cows descended
from the common parent should be suspected. At least 1/. of
them may be carriers.
Crampy cows tend to graze less than normal cows, because
of the inconvenience of walking which they suffer under attacks.
The condition becomes more severe with age. Life span may
be shortened and productiveness lessened under usual dairy farm
practices.
Selection of bulls for natural service or artificial use needs to
be considered, particularly by the breeder whose herd is a source
of seedstock. A crampy bull or carrier should not be used on







Florida Agricultural Experiment Stations


cows of similar genetic constitution. If a cow in a herd is crampy
and not above the average, her progeny do not justify being re-
tained for breeding purposes. A crampy bull whose daughters
are no better than their dams in production does not justify
being continued in service if he can be replaced with a normal
bull that is his equal. The distribution of this character can be
reduced and eliminated gradually among female stock in a herd
by breeding continually to bulls whose backgrounds are known
to be free of the gene.

SUMMARY AND CONCLUSIONS
Records were analyzed of 12,387 dairy bulls of 5 breeds, in
addition to 448 bulls of a dual-purpose and 3 beef breeds. Crampy
or progressive posterior paralysis occurred in both bulls and cows
3 years or older. The 323 affected dairy and 10 bulls of other
breeds represented 2.6 percent of the population studied. Fa-
milial relationships within the 5 dairy breeds indicated that the
character was hereditary. From the pattern of transmission,
the character appeared to be conditioned by a single autosomal
recessive gene with incomplete penetrance that becomes mani-
fest in homozygous condition in mature cattle. It was not pos-
sible, however, to rule out the possibility that the character could
be of multiple gene inheritance.
Frequency of occurrence differed significantly (P < 0.01)
among the dairy breeds. The last effective natural service or
semen collection from these bulls was at a mean age of 10.02
2.49 years. Some 19.5 percent of them died or were sacrificed,
and hence returned no salvage value to the owners.
Numerous familial relationships were established by pedigree
analysis. Differences of frequency of occurrence in sire groups
and in ';.- and line-crosses rejected significantly (P < 0.04
and P < 0.01, respectively) an hypothesis of random occurrence
of the condition. Thus a genetic background was established.
Although a multiple gene relationship was not discounted, inheri-
tance was suggested as a single recessive factor with incomplete
penetrance. If it is controlled by a single recessive gene, the dis-
tribution under a system of random matings would be that for
each 2.6 percent of potential crampy animals born, there could
be 27.1 percent of heterozygous carriers and 70.3 percent of the
population free from the recessive gene.
The gene (s) for crampy may well have been present in cattle
during the feudal period or earlier, to account for its distribution








Progressive Posterior Paralysis in Mature Cattle


in foundation cattle before development of these 9 improved
breeds.
Practical considerations are suggested as to cattle breeding.
This hereditary defect is distributed widely, and occurs among
some bloodlines regarded highly for transmitting milk and but-
terfat production. It can shorten the useful life and limit the
grazing ability of cattle.

ACKNOWLEDGEMENTS
Owners, farm managers and herdsmen in 48 states and most
Canadian provinces replied to inquiries concerning reasons for
disposal and causes of death of registered dairy bulls in natural
service. Similar reports were obtained from artificial breeding
organizations in both countries. The herdbook organizations
have cooperated in completing some records when needed. P. T.
Dix Arnold was a joint leader of the station project from Septem-
ber 1931 to June 1959. Bruce McKinley, and later A. H. Spur-
lock, are joint leaders of the phase dealing with dairy cows in
Florida herds. C. J. Wilcox succeeded P. T. Dix Arnold in July
1959. J. M. Wing photographed H-21 in Figure 1.
The National Association of Artificial Breeders has contrib-
uted toward support of the project since 1954. All dairy breed
associations have cooperated.

LITERATURE CITED
1. ANDERSON, W. A., and C. L. DAVIS. Congenital Cerebellar Hypoplasia
in a Holstein-Friesian Calf. Jour. Amer. Vet. Med. Assoc. 117:
460-461. 1950.
2. ANONYMOUS. Oral statements to the authors in 1960.
3. ARNOLD, P. T. DIX, R. B. BECKER, and A. H. SPURLOCK. Dairy Cattle
and Their Care. Fla. Agri. Exp. Sta. Bul. 599. 1958.
4. BECKER, R. B. Life Span of Bulls in A. I. Proc. 13th Ann. Cony. Natl.
Assoc. Artif. Breeders. 1960. Pages 77-84.
5. CHRISTIANSEN, E., and N. 0. CHRISTIANSEN. (Convenital Hereditary
Lameness in Calves. A Clinical and Pathological-anatomical In-
vestigation). Nord. Vet. Med. 4: 801-878. 1952.
6. COLE, L., and S. V. H. JONES. The Occurrence of Red Calves in Black
Breeds of Cattle. Wise. Agri. Exp. Sta. Bul. 313. 1935.
7. CULLEY, G. Observations on Live Stock. London. 1786.
8. DALE, D. G., and J. E. MOXLEY. Prenatal Tendon Contracture in a
Herd of Milking Shorthorns. Canadian Jour. Comp. Med. 16: 399-
404. 1952.
9. Dow, R. S. Partial Agenesis of the Cerebellum in Dogs. Jour. Comp.
Neurol. 72: 569-586. 1940.








Progressive Posterior Paralysis in Mature Cattle


in foundation cattle before development of these 9 improved
breeds.
Practical considerations are suggested as to cattle breeding.
This hereditary defect is distributed widely, and occurs among
some bloodlines regarded highly for transmitting milk and but-
terfat production. It can shorten the useful life and limit the
grazing ability of cattle.

ACKNOWLEDGEMENTS
Owners, farm managers and herdsmen in 48 states and most
Canadian provinces replied to inquiries concerning reasons for
disposal and causes of death of registered dairy bulls in natural
service. Similar reports were obtained from artificial breeding
organizations in both countries. The herdbook organizations
have cooperated in completing some records when needed. P. T.
Dix Arnold was a joint leader of the station project from Septem-
ber 1931 to June 1959. Bruce McKinley, and later A. H. Spur-
lock, are joint leaders of the phase dealing with dairy cows in
Florida herds. C. J. Wilcox succeeded P. T. Dix Arnold in July
1959. J. M. Wing photographed H-21 in Figure 1.
The National Association of Artificial Breeders has contrib-
uted toward support of the project since 1954. All dairy breed
associations have cooperated.

LITERATURE CITED
1. ANDERSON, W. A., and C. L. DAVIS. Congenital Cerebellar Hypoplasia
in a Holstein-Friesian Calf. Jour. Amer. Vet. Med. Assoc. 117:
460-461. 1950.
2. ANONYMOUS. Oral statements to the authors in 1960.
3. ARNOLD, P. T. DIX, R. B. BECKER, and A. H. SPURLOCK. Dairy Cattle
and Their Care. Fla. Agri. Exp. Sta. Bul. 599. 1958.
4. BECKER, R. B. Life Span of Bulls in A. I. Proc. 13th Ann. Cony. Natl.
Assoc. Artif. Breeders. 1960. Pages 77-84.
5. CHRISTIANSEN, E., and N. 0. CHRISTIANSEN. (Convenital Hereditary
Lameness in Calves. A Clinical and Pathological-anatomical In-
vestigation). Nord. Vet. Med. 4: 801-878. 1952.
6. COLE, L., and S. V. H. JONES. The Occurrence of Red Calves in Black
Breeds of Cattle. Wise. Agri. Exp. Sta. Bul. 313. 1935.
7. CULLEY, G. Observations on Live Stock. London. 1786.
8. DALE, D. G., and J. E. MOXLEY. Prenatal Tendon Contracture in a
Herd of Milking Shorthorns. Canadian Jour. Comp. Med. 16: 399-
404. 1952.
9. Dow, R. S. Partial Agenesis of the Cerebellum in Dogs. Jour. Comp.
Neurol. 72: 569-586. 1940.








Florida Agricultural Experiment Stations


10. DUERST, J. U. Kulturhistorische Studien den schweizerischen Rind-
viehzucht. Landwirt. Monathefte, Bern-Bumpliz. 1928.
11. FINCHER, M. C., et al. Diseases of Cattle. Chapter 10. The nervous
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12. FINLEY, K. H. An Anatomical Study of Familial Olivo-ponto-cerebellar
Hypoplasia in Cats. Proc. Sect. of Sciences. Kon. Akad. Wetensch.
Amsterdam. 38: 922-931. 1935.
13. FORMSTON, C., and E. W. JONES. A Spastic Form of Lameness in
Friesian Cattle. Vet. Rec. 68: 624-627. 1956.
14. FRAUCHIGER, K., and W. HOFMANN. Die Nervenkrankheites des Rindes.
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17. GOTZE, R. Spastische Parese der Realem Extremitaten bei Kalbern und
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19. HIPPEN, F. Erbbiplogische Untersuchungen der Fohlenatoxie im Old-
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20. HUTT, F. B. A Hereditary Lethal Muscle Contraction in Cattle.
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23. JENNINGS, A. B., and G. R. SUMMER. Cortical Cerebellar Disease in
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Pages 64-67. Iowa State College Press, Ames. 1945.








Progressive Posterior Paralysis in Mature Cattle


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