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Journal Title: American Journal of Veterinary
Research
Volume: 45
Issue: 7
Month/Year: Jul 1984
CJ)
z
Pages: 1455-9
~
Copyright Notice: This material may be
protected by Copyright law
(Title 17 U.S. Code)
Scanned with Adobe Acrobat & saved to K by:
Article Auth~r: Lawle r DF1, Monti KL.
Article Title: Morbidity and mortality in neonatal
kittens.
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Customer Information: [email protected]
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OS DB:
rk, Ap-
vitro
nosa to
lene.s . An1, 1980.
h
.erican
lliams
cterial
echa)-217,
B, Jr:
tetrai\-tro-
>tRes
~ ,Jr:
oxyTAand
982.
19. Moellering RC: Antimicrobial synergism-an elusive concept. J Infect Dis 140:63S641, 1979.
20. Norden, CW: Problems in determination of antibiotic synergism in vitro. Rev Infect Dis 4:276-281, 1982.
21. Weinstein RJ, Young LS, Hewitt WL:
Comparison of methods for assessing in vitro
antibiotic synergism againstPseudomonas and
Serratia. J Lab Clin Med 86:853-862, 1975.
22. Wooley RE, Jones MS, Gilbert JP, et
al: In vitro action of combinations of antimicrobial agents and EDTA-tromethamine on
Pseudomonas aeruginosa . Am J Vet Res
44:1521-1524, 1983.
23. Norden CW, Wentzel H, Keleti E: Comparison of techniques for measurement of in
vitro antibiotic synergism. J Infect Dis
140:629-633, 1979.
24. Dezeeuw JR: Accumulation of tetracyclines by Escherichia coli. J Bacteriol 95:498506, 1968.
25. Chopra I, Howe TGB : Bacterial resistance to tetracyclines. Microbial Rev 42:707724, 1978.
26. Yuan D, Shen V: Stability ofribosomal
and transfer ribonucleic acid in Escherichia
coli BN after treatment with ethylenedinitrilotetraacetic acid and rifampin. J Bacterial
122:425-432, 1975.
Morbidity and mortality in neonatal kittens
Dennis F. Lawler, DVM, and Katherine L. Monti, PhD
SUMMARY
The mortality patterns of 294 Domestic Shorthair kittens indicated
that birth weight was closely related
to survivability.
Slightly over half of the nonsurviving kittens lost at 0 to 3 days of
life were stillborn. Abnormal gross
anatomy did not appear to be a major factor in neonatal kitten death.
Mortality was lowest at the 5th parity and in litters of 5 kittens. Litters
of 1 kitten experienced high mortality. Smaller queens tended to deliver
fewer kittens per litter, but with improved kitten viability. Overweight
queens experienced increased mortality of kittens. Further examina, tion of mortality by litter size also
revealed that low birth weight kittens tended to survive less often than
normal birth weight kittens, even
within the same litter.
j
The importance of cats as both
companion and laboratory animals
has led to a marked increase in the
number of veterinarians skilled in
feline medicine and surgery, and an
expanding volume of knowledge
about feline biology and husbandry.
Therefore, many advancements
in feline colony medicine and management have been possible. The
literature contains a number of descriptions of housing facilities and
management procedures detailing
these improvements. 1 · 13
In spite of this, however, kitten
mortality continues to be a problem.
This is particularly true of neonatal
kittens. 14 ' 15 There is relatively little
available information concerning feReceived for publication Mar 9, 1983.
From the Departments of Pet Nutrition and Care
Research (Lawler) and Statistical and Data Services
(Monti), Ralston Purina Co, Checkerboard Square,
St Louis, MO 63164.
Am J Vet Res, Vol 45, No. 7
July 1984
line neonatal mortality. Differences
in husbandry and genetics, as well
as the various goals of breeding colony efforts, make comparative evaluation of existing data difficult .
However, kitten losses do appear to
exceed losses of the young of most
other laboratory animal species. 10
The purpose in the present report
is to describe kitten mortalities in a
large breeding colony over a 4 year
period.
Materials and Methods
The breeding colony consists of approximately 120 Domestic Shorthair
queens with an annual kitten production
of well over 400. The population was
originally established from specificpathogen-free (SPF) stock. The gene pool
has been modified as needed through periodic addition of breeding stock from
various SPF sources.
The colony is a barrier facility and is
maintained as a minimal disease, but not
SPF, environment. The environmental
conditions include a 22 C ambient temperature, 40% to 60% relative humidity,
17 air exchanges/hour, and a 14:10 hour
daily (light/darkness) cycle. These conditions generally agree with published
recommendations for the desirable environment for a feline colony. 5 -8 All cats
are vaccinated regularly against feline
panleukopenia, rhinotracheitis, and calicivirus infections.
Breeding is conducted on a harem (colony) basis, with 7 to 10 queens in a room
with 1 tom. Queens are palpated every
2 to 3 weeks to determine and monitor
pregnancy status. They are caged individually from approximately the 7th week
of gestation through parturition and kept
with their kittens during the nursing period until w~ aning (6 weeks old). Queens
are not used in reproduction after they
reach 8 years of age. Strict segregation
of cats by life stage and reproductive
status is maintained.
Physical examinations are conducted
during each queen's reproductive cycle
and during the nursing and growth periods of kittens. Breeding toms are examined at least 4 times a year. The body
weights of toms, queens, and kittens are
recorded weekly. Normal birth weight for
kittens is considered to be 100 g ± 10
g. 16 Kittens are weighed before 16 hours
of life; 90 g or more is considered to be
normal.
Dead kittens are either necropsied immediately after death or are refrigerated
and necropsied usually within 16 hours.
The necropsy report for each kitten identifies the sire and dam, dates of birth and
death, body weight at birth and death,
clinical or behavioral observations, and
the necropsy findings.
In addition to the necropsy information obtained (Tables 1 to 3), colony records were examined to determine whether
potential contributing factors to kitten
mortality in general could be identified
(Tables 2 and 4 to 8).
Results
Of the 294 kitten mortalities, 267
were either stillborn or died by age
3 days. Three days defined the immediate neonatal period because cats
in this colony usually do not die from
congenital or other birth-related
problems after this time.
Among these 267 neonatal mortalities, 25 were cannibalized and 10
were autolyzed. Of the remaining 232
kittens, 125 (54%) were stillborn and
107 (46%) were born alive and subsequently died. Ninety-two (40%) had
normal birth weight and 138 (59%)
were small; 178 (77%) were anatomically normal, and 47 (20%) had 1 or
more anatomic abnormalities (Table
1).
Of the 125 stillborn kittens, 93 had
normal gross anatomy at necropsy;
46 of these 93 kittens had inadequate body weight. Twenty-seven
stillborn kittens had abnormal gross
anatomy, and 18 of these had inadequate body weight (Table 1).
Of the 107 live-born kittens, 85 had
normal gross anatomy at necropsy.
Of these 85 kittens, 62 had inadequate body weight. Twenty live-born
kittens had abnormal gross anat1455
TABLE 1-Distribution of 294 nonsurviving kittens subjected to necropsy
Normal anatomy
Item
Neonatal (n = 267) 0-3 days
Stillborn (n = i25)
Liveborn (n = i07)
Cannibalized (n = 25)
Autolyzed (n = iO)
Nursing (n = 27) 4-42 days
Abnormal anatomy
Normal
birth weight
Low
birth weight
Normal
birth weight
47
23
46
62
9
9
i9+
2:j:
3:j:
i8
11
TABLE 2-Body weight comparison of nonsu
s1blrngs
Undetermined
Low
birth weight
Normal
birth weight
Low
birth weight
4
i
-t
-t
Item
Died
Survived
x2
Low body
weight(%)
i38 (60)
54 (22)
i85.97, p < 0.0001.
TABLE 3-Congenital defects (n - 51 kittens
3*,:j:
* = One possible acquired defect. t = Birth weight unknown for 2 liveborn kittens. :j: = Categorized by death weight. - = Not applicable.
omy, and 11 of these had inadequate
body weight (Table 1). Therefore,
kittens with low birth weight constituted a high percentage of each
category examined.
Table 2 compares 477 surviving
and nonsurviving kittens grouped by
birth weight and shows a highly significant difference in survival between the low birth weight and
normal birth weight kittens.
Table 3 shows the specific anatomic abnormalities encountered (in
descending order of frequency of occurrence). In this series, cleft palate
occurred most frequently, followed by
exencephaly and agenesis of the intestinal tract. Several kittens had
multiple abnormalities, the greatest
number in any one kitten being 3,
which o<;:curred only once.
Twenty-five neonatal kittens were
cannibalized; therefore, complete
evaluation was not possible. However, several of these were established as either stillborn or live-born,
and of low or normal birth weight,
indicating an absence of a consistent
pattern. In the majority of cases, the
queens involved were of nervous
temperament. Ten neonatal kittens
were sufficiently autolyzed to preclude making any evaluation.
The only sex-associated data in the
study revealed that 75% of the anatomically abnormal live births were
female kittens.
Twenty-seven kittens died between 4 and 42 days of age. Five of
these were anatomically abnormal,
and 22 had subnormal body weight
at the time of death (Table 1). The
recognized causes of death in this
group were predominately acquired
problems, with trauma and septicemia being the most frequent diagnoses where a diagnosis was made.
In several of these kittens, no diagnosis was established, One of the anatomic abnormalities in this group
was a fistula between the colon and
the urinary bladder, and it may have
been an acquired problem.
1456
Colony records were reviewed to
examine the influence of the following variables on kitten mortality:
parity, litter size, kitten size within
1itters, queen body weight, and sire
(Tables 4 to 8).
Only queens having 4 or more litters were included in Tables 4, 5, and
7. Litters included in Table 8 differ
slightly from those in Tables 4 to 7,
since individual kitten weight records were not available in certain instances. Also, the time period of
necropsy data collection differed
slightly from the period from which
colony historical data was collected.
In the analysis of the data in Tables 4 through 8, multivariate statistical relationships among the
values are not examined. When statistical models including the effects
for individual queens were used to
explore more complex relationships
among the values, the trends found
were similar to the univariate trends
which are reported. When combinations of variables were considered simultaneously, the sample sizes
became too small to support meaningful statistical interpretation.
Table 4 indicates that the overall
losses and the percentage of litters
experiencing losses were lowest at the
5th parity, with the greatest percentage of litters experiencing some
loss at the 7th parity. Litter size was
greatest at parity 2, which somewhat offset the 21.9% mortality level.
Table 5 indicates that smaller
queens tended to have fewer kittens
per litter, but improved kitten viability. Intermediate-sized queens
weaned slightly more kittens per litter by virtue of larger litter sizes, but
actually had higher kitten mortality
than 2.7 to 3.1 kg queens. The heaviest queens (4.1-4.5 kg) also experienced increased kitten losses. These
queens were frequently diagnosed as
obese upon physical examination, and
were usually older as well. However,
the sample size was smaller in the
heaviest weight category.
In Table 6, litter size and percentage of mortality are examined by sire,
with 6 of the colony's more active
sires represented. Sires A and C experienced higher mortality of kittens sired and a tendency toward a
smaller mean litter size, suggesting
diminished reproductive capacity.
Table 7 reveals that litters of 1
kitten experienced unusually high
losses, with almost half failing to
survive. Litters of 7 kittens also experienced a slight increase in overall
mortality, although again the sample size was small. Some losses were
suffered in a high percentage of litters of both 6 and 7 kittens, which
presented only a slight advantage in
terms of actual kittens weaned. The
lowest percentage of mortality was
in litters of 5 kittens, whereas the
lowest perc~ntage of litters experiencing some loss was in litters of 2
kittens.
Table 8 demonstrates that among
litters ranging from 1 to 7 kittens,
smaller kittens had a uniformly
higher death rate when compared
with normal birth weight kittens in
litters of the same size.
Discussion
Birth status-The neonatal period
has been recognized in dogs as crit·
ical to puppy survival. 11 •18 Our data
for kittens revealed that 91 % of
preweaning losses occurred in the
immediate neonatal period, with
slightly over half being stillborns.
Postweaning losses are few in this
colony, probably due to the devel·
opment of strict sanitation and man·
agement practices. Losses between
implantation and parturition can be
significant in some queens,a but lit·
tle quantified information is available.
In addressing postweaning dis·
ease control in a closed breeding col·
ony, an earlier study reported 9.3%
• Wildt D, National Institutes of Health, Bethesda, Md: Personal communication, i982.
Am J
Vet Res, Vol 45, No. 7
Defects
Cleft palate
Exencephaly*
Agenesis of small and large bowel
Schistosomas
Limb deformity
Atresia ani
Tail absent
Renal hypoplasia, unilateral
Renal hypoplasia, bilateral
Stubtail
Scoliosis
Cardiac anomaly
Fused pelvic kidneys
Umbilical hernia, nontraumatic
Diaphragmatic hernia
Hydrocephalus
Total no. of occurrences
(kittens 0 to 6 weeks of age)
*Kittens with exencephaly usually have cleft pall
These are not mcluded in the 23 cases of cleft palate
neonatal deaths and a total of 15%
deaths
by age 7 days for a 1-year pe. d : 11 A n extensive general survey
no
of kitten mortality 14 and a study of
laboratory breeding and management of felines 12 also demonstrated
~he p~oblem presented by preweanmg kitten mortality. It is apparent
that the neonatal and nursing periods represent a crisis for kittens and
it is not surprising that the neo~atal
kitten is at especially high risk.
Sex-It was noted that 75% of the
anatomically abnormal live births
we~e female kittens, the only sex-associated data in this study. However, because of the comparatively
sm~ll size of this group, an attempt
at mterpretation was not made.
Anatomic status-The most commonly seen gross anatomic defects
were cleft palate(23), exencephaly(15), and agenesis of the intestinal tract(7). Exencephaly is a
combination of defects about the face
~nd head, inclu?ing a dorsal opening
1~ the skull with protruding brain
tissue, large ears, bulging eyes, and
cleft palate. 19-2 1 Associated vertebral
column defects may be noted and
were observed once in our series in
a k~tt:n with exencephaly, sev~re
scoliosis, and schistosomas reflexus.
This was the only kitten in the seJuly 1984
•
TABLE 2-Body weight comparison of nonsurviving kittens and surviving
siblings Normal body
Low body
weight(%)
weight
Item
ht
J
'I
138 (60)
54 (22)
Died
Survived
x2
= 185.97, P
<
92
193
o.oooi.
TABLE 3-Congenital defects (n = 51 kittens)
Defects
Cleft palate
Exencephaly*
Agenesis of small and large bowel
Schistosomas
Limb deformity
percent! by sire,
e active
nd C ex1 of kitoward a
Atresia ani
Tail absent
Renal hypoplasia, unilateral
Renal hypoplasia, bilateral
Stubtail
~gesting
iacity.
ers of 1
ly high
Hing to
also ex1 overall
he sam;es were
re of lit:, which
1 tage in
ed. The
ity was
1e as the
experiers of 2
among
kittens,
formly
mpared
;tens in
neonatal deaths and a total of 15%
deaths by age 7 days for a 1-year period.11 An extensive general survey
14
~ of kitten mortality and a study of
( laboratory breeding and management of felines 12 also demonstrated
the problem presented by preweaning kitten mortality. It is apparent
that the neonatal and nursing periods represent a crisis for kittens, and
it is not surprising that the neonatal
kitten is at especially high risk.
l1
I
Sex-It was noted that 75% of the
anatomically abnormal live births
were female kittens, the only sex-associated data in this study. However, because of the comparatively
small size of this group, an attempt
at interpretation was not made.
!.
Anatomic status-The most commonly seen gross anatomic defects
were cleft palate(23), exencephaly(l5), and agenesis of the intestinal tract(7). Exencephaly is a
combination of defects about the face
and head, including a dorsal opening
in the skull with protruding brain
tissue, large ears, bulging eyes, and
cleft palate. 19-21 Associated vertebral
column defects may be noted and
were observed once in our series, in
a kitten with exencephaly, severe
scoliosis, and schistosomas reflexus.
This was the only kitten in the se-
i, No. 7
July 1984
~tween
can be
mt litavailtg disng col:l 9.3%
alth, Be-
23
15
Parity
Litter size
1
2
3
4
4.0
4.6
3.6
3.9
Av. No. of
kittens weaned/
litter
3.2
3.5
3.0
3.1
5
6
7
3.8
3.7
3.8
3.4
2.7
2.7
No. of Percentage
litters mortality
22.2
37
37
21.9
37
23.6
18.0
35
27
21
16
Percentage of
litters experiencing
losses
12.6
29.4
26.5
43.2
45.9
45.9
42.9
33.3
42.9
56.2
*Queens with 4 litters or more.
7
3
3
2
2
1
1
1
Scoliosis
Cardiac anomaly
Fused pelvic kidneys
Umbilical hernia, nontraumatic
Diaphragmatic hernia
Hydrocephalus
Total no. of occurrences
64
(kittens 0 to 6 weeks of age)
*Kittens with exencephaly usually have cleft palate among other defects. 1• · 2 1
These are not included in the 23 cases of cleft palate listed.
I
period
as crit1r data
H% of
in the
, with
lborns.
in this
develd man-
No. of
occurences
TABLE 4-Kitten percentage of mortality by parity*
TABLE 5-Kitten percentage of mortality by queen weighl*
Body wt Mean Mean No. of kittens Percentage Percentage of litters No. of
litter size weaned per litter
mortality experiencing losses litters
(kg)
23.8
21
12.6
2.7-3.1
3.4
3.0
38
19.2
4.0
3.2
3.2-3.6
36.8
13
20.9
5.0
4.2
3.7-4.0
61.5
40.0
8
3.8
2.5
4.1-4.5
62.5
* Queens with 4 litters or more.
TABLE 6-Kitten percentage of mortality by sire
Item
Mean kitten mortality (%)
Mean litter size
ries exhibiting more than 2 gross anatomic defects.
The birth defects noted in Table 3
and categorized in Table 1 usually
occurred as a single event or multiple events in 1 litter, but were not
usually repeated in subsequent matings of the same sire and dam. Examination of the previous breeding
records of cats in these situations also
revealed no obvious familial relationshi_ps, with 1 exception. There
was no particular pattern of associated defects noted in those kittens
with multiple anatomic abnormalities. Since data beyond the historical information and subsequent
matings are lacking, no further
evaluation concerning the genetic
implications of these anatomic defects is reported. Among postweaning kittens and adult cats in the
present colony, anatomic defects are
uncommon and have usually been
incidental findings at a surgical intervention or at necropsy. In the colony, queens or sires with a history
of producing kittens with anatomic
defects in multiple litters are removed from breeding service, and
surviving offspring are also excluded from breeding.
Our data and previous work 10 •14
indicate that while gross anatomic
defects are certainly responsible for
some kitten losses, they are proba-
Sire
A
35.9
3.5
Sire
B
22.1
3.9
Sire
c
37.3
3.2
Sire
D
15.7
5.0
Sire
E
Sire
20.1
3.4
20.6
4.3
F
bly not the overriding cause for neonatal mortality when proper genetic
management procedures are applied. An excellently referenced
summary of feline congenital defects
is available. 19 Metabolic disorders not
resulting in gross anatomic defects
were not explored in this study, but
this emerging area of research holds
the potential for better diagnosis of
the causes of neonatal mortality in
the future. 22
Birth weight-Kittens with low
birth weight constituted a high percentage of live-born and stillborn
categories, irrespective of anatomic
status (Tables 1 and 2). The large
number of low birth weight kittens
in the nonsurviving group was significantly different from a similar
sized group of surviving kittens.
The low birth weight, nonsurviving kittens were usually weak, if born
alive, and appeared to be ineffective
nursers. Activity was markedly reduced and the kittens frequently became hypothermic and dehydrated.
These live-born kittens usually lost
weight between birth and death, often
in excess of that expected from simple dehydration. Queens frequently
attempted to care for these failing
kittens; maternal neglect was uncommon. At necropsy, a complete lack
of body fat was usually noted, and
1457
TABLE 8-Kitten percentage of mortality: Kittens within litters
TABLE ?-Kitten mortality by litter size*
Litter size
1
2
3
4
Kittens weaned
per litter
0.53
1.57
2.24
3.18
5
6
7
* Queens with 4
4.35
4.76
4.75
litters or more.
Percentage
mortality
47.1
21.4
25.2
20.6
Percentage of litters
experiencing losses
47.1
32.1
43.2
39.2
No. of
litters
17
28
37
74
13.0
20.6
32.1
45.7
64.7
75.0
46
17
8
No. of
litters
22
27
51
66
40
8
4
Litter size
1
2
3
4
5
6
7
Small-sized kittens
Percentage Percentage of
of kittens
mortality
50.0
63.6
60.0
29.6
33.3
55.6
47.8
33.3
28.5
57.3
52.1
31.7
46.4
57 .1
the stomach and intestines were
empty, confirming the clinical
impression of ineffective nursing.
In an earlier study of 1st-parity
kittens, the total preweaning losses
of only 8% to 9% were accompanied
by a high mean birth weight of 109
g. 10 A 2nd study reported high survivability in a group of 43 kittens
with a similar mean birth weight. 13
It is clear that low birth weight bears
a significant relationship to mortality in neonatal kittens.
Approximately 40% of the neonatal losses, however, did have normal
birth weight. Many of these were also
anatomically normal, whether stillborn or live-born. Clinical and necropsy observations indicated that
birth canal trauma or other dystocia
accounted for some of the deaths in
this group. This usually involved
large kittens carried to term by a
small or 1st-parity queen, but the
number of kittens which might be
placed in this group still did not account for most of these deaths.
Body weight of queen-Smaller
queens (2.7-3.1 kg) tended to have
fewer kittens per litter, a fact which
was noted in an earlier study 23 and
which might be important where
kitten production requirements are
high. However, it should also be noted
that larger queens appeared to experience greater kitten losses, which
were somewhat offset by their larger
litter sizes. The heaviest group (4.14.5 kg) experienced both decreased
litter sizes and greater kitten losses.
Parity-The data indicate that an
optimum of reproductive efficiency
occurs at the 5th parity. A few of the
queens excluded from Tables 4, 5, and
7 were too young to have achieved
4th parity during the study period,
and others had been removed due to
poor reproductive performance. Inclusion of the latter group of queens
would have raised 1st-parity mortality. Thus, the percentage of mortality at 1st parity was slightly
higher than Table 4 indicates.
The queens included in Table 4
were approximately 1 year of age at
1st parity. A group of 20 queens, not
a part of this study and not retained
through the 4th parity, were more
than 3 years of age at 1st parity.
These queens experienced high kitten losses, indicating that the age of
the queen upon entering reproductive service also may influence kitten mortality.
Due to higher kitten mortality and
the fact that overweight queens frequently also experience reproductive disorders, such as infertility,
subfertility, prolonged parturition,
or dystocia, these queens are usually
not maintained for reproductive purposes in our colony, regardless of age.
1458
Insufficient data were available for
queens weighing less than 2. 7 kg, but
the available data would suggest
that, for queens in our colony, optimal reproductive efficiency is obtained at queen body weights from
2.7-3.1 kg. Since many queens tend
to gradually gain weight during their
reproductive years, it is difficult to
separate queen age and weight effects on kitten viability from our data.
Queens weighing over 4.1 kg were
generally considered to be frankly
obese and were usually older.
Sire-Interestingly, both of the
Table 6 toms experiencing poor production were later removed from reproductive service-1 because of
chronic and progressive renal dysfunction and 1 because of gradually
advancing infertility. Infective agents
were not identified in either tom.
These observations underscore the
need to maintain close surveillance
of all breeding animals for genetic
performance, as well as for slowly
progressive, chronic disorders which
may eventually directly or indirectly affect fertility.
Normal-sized kittens
Percentage Percentage of
mortality
of kittens
27.3
50.0
23.8
70.4
66.7
14.6
66.7
18.5
11.8
71.5
47.9
16.7
53.6
27.8
Litter size-The reason for the high
losses of kittens in litters of 1 is not
totally clear, but may relate to factors which disrupt the early development of other fetuses in these
litters, resulting in their reabsorption. a Except for the decreased losses
in litters of 5, mortality in litters of
2 through 6 kittens was similar, with
a slight increase noted in litters of 7
(Table 7). Little data were available
for litter sizes above 7, but examination of colony records which were
available suggested continuation of
the rise in mortality in unusually
large litters. It would appear that selection of breeding queens for large
litter size only has some limitations.
Kittens within litters-Table 8
supports the direct relationship between low birth weight and mortality noted in the examination of the
necropsy data. The percentage of
small- and normal-sized kittens
which did not survive ranged from
31.7 to 63.6% and from 11.8 to 2'7.8%,
respectively, when examined by litter size. Further, examination of individual reproduction records showed
that, within individual litters, small
kittens tended to die, whereas larger
siblings were much more likely to
survive.
Low birth weight in newborn puppies is usually considered to be accompanied by physiologic immaturity
and appears to be an important determinant of puppy survival. 24 Some
suggested causes of neonatal pup
mortality include infections, genetics, environment, nutrition, metabolic dysfunction, and immature
thermoregulatory mechanisms, any
of which may be ·superimposed on
immature cardiopulmonary function. 17 •18 It seems reasonable to suggest that somewhat similar factors
also may have a role in kitten mor- '
tality, although this area requires
investigation.
From a management standpoint,
it is important to remove queens
Am J
Vet Res, Vol 45, No. 7
consistently delivering low birth
weight kittens from a breeding program if a correctable nongenetic under lying cause cannot be found. 4
Clinical observations have indicated
that some kittens with low birth
weight survive the neonatal period
and become chronic "poor-doers,"
which succumb during the later
nursing period or during the immediate postweaning period. Others
survive to adulthood, but usually do
not attain the expected body size and
weight. It should be noted that 22 of
the 27 kittens dying between 4 and
42 days of age were subnormal in
body weight at the time of death, although many were normal at birth.
In these instances, an acquired problem was usually present, or no diagnosis was made.
Cannibalism, in the authors' experience, is relatively uncommon and
usually involves only an occasional
kitten or litter. Cannibalism of repeated litters by one queen should
prompt removal of the queen from a
breeding program. 4 When cannibalism becomes a problem in a cattery,
breeding and management procedures should be examined carefully.
Nervous temperament in the queen
appeared to be involved in most instances of cannibalism in this series,
and clinical observations also have
suggested that older queens tend to
cannibalize kittens with a slightly
greater frequency.
Factors, such as those detailed in
Tables 4 to 8, must also be carefully
considered and it must be recognized
that complex interrelationships may
exist among quantifiable and non-
July 1984
quantif
genetics
Vario
colonies
onies, a
may diff
pattern
manag
greater
cat bree
tain acc
obtain n
survivin
base suf
underst
mortalit
exist in
ject.
Referen
1. Whi
Housingre
EC Jr, Alt
ratoryAnim
1974, Vol
2. Patt
(ed): Anima
York, Acad
3. Keal
DA Ced): Cu
Philadelph
860.
4. Scott
duction ano
ratory Anim
1970, pp 19
5. Scott
tion in the a
by increasin
1959.
6. Piphe
design. Lab
7. Alsen
search ani
13:321-329,
8. US D
and Welfan
of mortality: Kittens within litters
-sized kittens
Normal-sized kittens
:e Percentage of Percentage Percentage of
mortality
of kittens
mortality
63.6
50.0
27.3
60.0
70.4
23.8
55.6
66.7
14.6
47.8
66.7
18.5
57.3
71.5
11.8
31.7
47.9
16.7
57.l
53.6
27.8
Litter size-The reason for the high
;ses of kittens in litters of 1 is not
;ally clear, but may relate to facs which disrupt the early develment of other fetuses in these
ers, resulting in their reabsorpn. a Except for the decreased losses
litters of 5, mortality in litters of
hrough 6 kittens was similar, with
light increase noted in litters of 7
ible 7). Little data were available
litter sizes above 7, but examiion of colony records which were
~ilable suggested continuation of
rise in mortality in unusually
ge litters. It would appear that sebon of breeding queens for large
er size only has some limitations.
'
[ittens within litters-Table 8
'p orts the direct relationship be!en low birth weight and mortalnoted in the examination of the
ropsy data. The percentage of
~ 11- and normal-sized kittens
lch did not survive ranged from
to 63.6% and from 11.8 to 2'7.8%,
)ectively, when examined by litize. Further, examination of inClual reproduction records showed
, within individual litters, small
ens tended to die, whereas larger
ings were much more likely to
ive.
t> w birth weight in newborn pupis usually considered to be acpanied by physiologic immaturity
appears to be an important de1inant of puppy survival. 24 Some
~ested causes of neonatal pup
tality include infections, gees, environment, nutrition, metic dysfunction, and immature
µioregulatory mechanisms, any
hich may be superimposed on
ature cardiopulmonary func17' 18 It seems reasonable to sugthat somewhat similar factors
may have a role in kitten mory, although this area requires
stigation.
om a management standpoint,
important to remove queens
Am J Vet Res, Vol 45, No. 7
I
'
ll
'J
•
(
1
consistently delivering low birth
weight kittens from a bi::eeding program if a correctable nongenetic underlying cause cannot be found. 4
Clinical observations have indicated
that some kittens with low birth
weight survive the neonatal period
and become chronic "poor-doers,"
which succumb during the later
nursing period or during the immediate postweaning period. Others
survive to adulthood, but Uf;)ually do
not attain the expected body size and
weight. It should be noted that 22 of
the 27 kittens dying between 4 and
42 days of age were subnormal in
body weight at the time of death, although many were normal at birth.
In these instances, an acquired problem was usually present, or no diagnosis was made.
Cannibalism, in the authors' experience, is relatively uncommon and
usually involves only an occasional
kitten or litter. Cannibalism of repeated litters by one queen should
prompt removal of the queen from a
breeding program. 4 When cannibalism becomes a problem in a cattery,
breeding and management procedures should be examined carefully.
Nervous temperament in the queen
appeared to be involved in most instances of cannibalism in this series,
and clinical observations also have
suggested that older queens tend to
cannibalize kittens with a slightly
greater frequency.
Factors, such as those detailed in
Tables 4 to 8, must also be carefully
considered and it must be recognized
that complex interrelationships may
exist among quantifiable and non-
July 1984
quantifiable variables relating to
genetics, health, and management.
Various purebreed catteries, SPF
colonies, conventional research colonies, and random-source colonies
may differ considerably in mortality
patterns. Genetics, disease, and
management factors may play
greater or lesser roles. Operators of
cat breeding colonies should maintain accurate mortality records and
obtain necropsy information on nonsurviving kittens to establish a data
base sufficient to provide a greater
understanding of feline neonatal
mortality. It is clear that many gaps
exist in our knowledge of this subject.
References
1. White WJ, Balk MW, Slaughter LJ:
Housing requirements - dogs and cats, in Melby
EC Jr, Altman AH (ed): Handbook of Laboratory Animal Science. Cleveland, CRC Press,
1974, Vol 1, pp 69--84.
2. Patterson JS: Cats, in Lane-Petter W
(ed): Animals for Research. London and New
York, Academic Press Inc, 1963, pp 417-436.
3. Kealy RD: Feline Nutrition, in Morrow
DA (ed): Current Therapy in Theriogenology.
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1970, pp 192-208.
5. Scott PP, Lloyd-Jacob MA: Reproduction in the anoestrus period oflaboratory cats
by increasing illumination. Nature 184:2022,
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Guide for the Care and Use of Laboratory Animals. Revised Edition, 1978.
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Anim Pract 11:533-543 , 1970.
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disease in a cat breeding colony. Lab Anim
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12. Lamotte JHL, Short DJ: The breeding
and management of cats under laboratory
conditions. J Inst Anim Tech 17:85- 96, 1966.
13. Bleby J , Lacey A: The establishment of
a specific pathogen free cat (Felis catus) colony. J Small Anim Pract 10:237-248, 1969.
14. Scott FW, Geissinger C, Paltz R: Kitten
mortality survey. Feline Pract 8:31-34, 1978.
15. Scott FW, Weiss RC , Post JE, et al: Kitten mortality complex (neonatal FIP?). Feline
Pract 9:44-56, Mar-Apr 1979.
16. Berman E : Growth patterns, fetal and
neonatal, in Morrow DA (ed): Current Therapy in T erioge nology . Philadelphia, WB
Saunders Co, 1980, pp 850-853.
17. Fox MW: The pathophysiology of neonatal mortality in the dog. J Small Anim Pract
6:243-254, 1965.
18. Fox MW: Neonatal mortality in the dog.
J Am Vet Med Assoc 143:1219-1223, 1963.
19. Saperstein G, Harris S, Liepold HW:
Congenital defects in domestic cats . (Reprinted from the Journal of Feline Practice
for the Ralston Purina Company with permission by Veterinary Practice Publishing
Company, 1978.)
20. Field B, Wanner RA: Cerebral malformation in a Manx cat. Vet R ec 96:42-43, 1975.
21. Sekeles E : Craniofacial and skeletal
malformations in a cat. Feline Pract 11:2831, Mar-Apr 1981.
22. Jezyk , PF : Metabolic diseases-an
emerging area of veterinary pediatrics. Compend Cantin Ed 5:1026-1032, 1983.
23. Hall VE, Pierce GN: Litter size, birthweight and growth to weaning in the cat. Anat
R ec 60:111-123, 1934.
24. Mosier JE: The puppy from birth to six
weeks, in Mosier JE (ed): Symposium on canine pediatrics. V et Clin North Am. Philadelphia, WB Saunders Co, 1978, pp 79-100.
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