Котешко кътче

R – Reproduction
SMALL ANIMAL NEONATOLOGY: THEY LOOK NORMAL WHEN
THEY ARE BORN AND THEN THEY DIE
Dr. Danielle Gunn-Moore
University of Edinburgh
Danielle.Gunn-Moore@ed.ac.u
Kitten deaths
Sadly, it is inevitable that some kittens will die,
and a low level of loss is to be expected, even
in the best run breeding cattery. It is generally
found that pedigree cats have higher levels
of neonatal mortality than non-pedigree. In
one study, pedigree cats had an average kitten
mortality of 34.5% from birth to one year of age
(range of 8-40%), compared to 10-17% in nonpedigree
cats. These higher levels of mortality
may refl ect inbreeding within pedigree cats.
However, there may also be bias in the nonpedigree
data as it is diffi cult to get accurate
fi gures for pet cats.
Kitten deaths can be divided into those occurring
in the pre-weaning period (stillbirths and deaths
in the fi rst 4 weeks of life), and those occurring
in the post-weaning period (deaths occurring
from weaning to ~6 months of age). Overall,
pre-weaning mortality is commonly 15-30%,
and stillbirths typically account for <10% of all
kittens born; although, the prevalence can vary
considerably; from 6-22% in pedigree cats.
Kitten mortality is highest in the fi rst week of
life (typically >90% of all kitten mortality),
after which it declines, only to rises again just
after weaning. Pre-weaning losses usually result
from non-infectious causes while infectious
causes are more prevalent post-weaning. This
is because prior to weaning the kittens are
relatively protected from infectious disease by
maternally derived antibody (MDA) (see section
on infectious disease for more information on
MDA). Kittens dying between birth and weaning
are frequently called ‘fading kittens’.
Neonatal kittens may die suddenly, or present
as ‘poor doers’ and ‘fade’ within a few days.
Unfortunately, the clinical signs of many
neonatal diseases are very similar and vague.
While normal kittens tend to cuddle together and
sleep contentedly between feeds, sick kittens
tend to lie separately, are generally more restless,
are not keen to suckle, and cry frequently (if still
strong enough to do so).
Neonates are vulnerable because their
thermoregulatory mechanisms are poorly
developed, they are at increased risk of
dehydration and hypoglycaemia, and they
are immunologically immature. Therefore,
regardless of the initiating cause, neonates
rapidly become hypothermic, hypoglycaemic,
dehydrated, hypoxic, and die. They are
predisposed to hypothermia because they
cannot thermoregulate, lack insulating fat and
thermogenic brown, cannot induce peripheral
vasoconstriction, cannot react to cold by
shivering, and have a large surface area to volume
ratio over which to loose body heat. Hypothermia
then triggers ileus and reduced intestinal
absorption, increases susceptibility to infection,
and eventually leads to cardiopulmonary failure.
Neonates are predisposed to hypoglycaemia
because they have high energy requirements (2-
3x the metabolic rate of adults/kg body weight),
but have no energy reserves and their immature
livers are ineffi cient at generating energy. This
can then be exacerbated by hypothermia-induced
reduction of intestinal absorption. The neonatal
risk of dehydration is because they have a higher
percentage of body water (82%) than adults,
while incurring greater loses through their
immature kidneys, lungs and skin.
Causes of ‘fading’ or sick kittens:
• Birth / queen-related factors (kitten hypoxia,
trauma, hypothermia)
• Congenital abnormalities
• Low birth weight
• Inappropriate environment (temperature,
humidity, hygiene, overcrowding, over-handling)
• Inappropriate nutrition
• Neonatal isoerythrolysis (NI)
vInfection (viral, bacterial, parasitic)
R This manuscript is reproduced in the IVIS website with the permission of WSAVA
2006 World Congress WSAVA/FECAVA/CSAVA
715
1. Birth / queen-related factors
Kittens that suffer dystocia have a signifi cantly
increased risk of death within the fi rst few weeks
of life. In fact, prolonged labour or dystocia are
probably the most signifi cant causes of neonatal
death. This results from the effects of hypoxia and/
or trauma. Dystocia occurs in ~6% of pregnancies
(range 0-18%). Studies have shown that cats with
extremes of conformation, such as the Siamese
and Persians, experience much higher levels of
dystocia (7-10%; see FAB Manual) than cats with
normal conformation (generally <5%). Hypoxia
during birth can result in stillbirth, or the birth
of weak, slow, kittens that fail to suckle. These
kittens usually die within the fi rst week of life or,
due to failing to ingest suffi cient colostrum, have
an increased risk of infectious disease.
Kitten mortality is usually highest in the fi rst litter
born to a particular queen and after her fi fth litter.
The high death rates in kittens from fi rst-time
queens probably relates to inexperience, trauma
and cannibalism. Older queens tend to have
smaller litters and tend to produce more kittens
with congenital defects. The negative effect of
extremes of litter size is seen as reduced survival
of single kittens, and of kittens from litters of
7 or more. Kitten mortality also increases with
increasing maternal obesity, and with other queenrelated
causes, including a lack of milk, mastitis,
or maternal neglect.
2. Congenital abnormalities
Obvious physical defects may be seen in 10-20%
of stillborn kittens. However, the prevalence
varies considerably; from 1-10% of kittens born to
research cats, to 1-31% of kittens born to pedigree
cats. Congenital disorders are present from birth,
and can affect any body system. They may result
from genetic disorders (see refs.) or teratogenic
factors. Because inbreeding increases the risk
of genetic disease, congenital disorders are seen
more frequently in pedigree cats. In addition,
certain defects are seen more frequently in some
breeds than others (see FAB Manual and refs.).
Congenital defects resulting from exposure to
teratogenic substances may be seen in cats of
any breed. For example, cleft palates may result
from treatment with griseofulvin, corticosteroids,
or excessive amounts of vitamin A; skeletal
deformities may result from the administration
of organophosphate anti-fl ea products. It has
also been suggested that overheating, in some
pregnant cats, may result in an increased risk of
skeletal deformity in their kittens. Severe defects
usually result in stillbirth or early neonatal death.
Milder disorders may result in fading kittens, or
only become apparent later in life.
3. Low birth weight
Underweight kittens have a signifi cantly
increased risk of neonatal death. They are
physiologically immature compared to normalweight
kittens, and they may be too weak to nurse
adequately. In addition, they lack insulating fat
and thermogenic brown fat, and they have weak
thoracic muscles and immature lung development.
They are particularly susceptible to hypothermia,
dehydration, respiratory failure, and sepsis.
Kittens may be born underweight because of
maternal malnutrition or ill-health; congenital
disease; in utero infections; or any condition that
results in poor placental blood supply. The average
birth weight for most breeds of cat is 100g ± 10g.
However, it is normal for some breeds to have
signifi cantly smaller kittens (Oriental; ave. 80g);
while others (Maine Coon) have signifi cantly
larger kittens (ave.120g) (see FAB Manual).
It is therefore very important to know what the
average weight for kittens of a particular breed is
when trying to decide whether or not a particular
kitten is underweight. As a general guideline
newborn kittens <75g are likely to have very high
death rates.
4. Inappropriate environment
Environmental factors, such as extremes of
temperature and humidity, poor hygiene,
overcrowding, or over-handling, all result in
increased kitten mortality. Ideally, the kittening
room should be well ventilated, draft free,
and maintained at a fairly constant 18-24oC,
55-60% humidity. This will allow the dam to be
comfortable, and she can supply any additional
heat required by the offspring. Where kittens
have to be hand-reared it is necessary to supply
additional heating. Ideally the temperature in
the box should be maintained at 29-32oC, but
the box should be large enough for the kittens to
move away from the heat if they become too hot.
The temperature is gradually reduced to 27oC by
7-10 days and 22oC by the end of the fi rst month.
Overcrowding will lead to increased infectious
disease and disease resulting from competition at
the mother’s nipples (which can in turn result in
inadequate nutrition [see below]). Over-handling
will not only limit the kitten’s feeding time, but
with nervous queens, may result in cannibalism
of her kittens.
Providing kittens with a suitable environmental
temperature is essential. A kitten that has ceased
to suckle regularly will quickly become cold and
hypoglycaemic. Since neonates cannot shiver and
are unable to control their own body temperature
hypothermia will result, and this will lead to a
further reduction in activity and suckling. The
rectal temperature of new-born kittens ranges
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from 35-37oC in the fi rst week, to 36-38oC in the
second and third weeks, and reaches normal adult
levels of 38-39oC by the fourth week.
Hypothermia is particularly harmful as it can
initiate a number of other problems. For example:
a week-old kitten should have a temperature
of 35-37oC and a heart rate of 200-250 bpm.
However, if its temperature falls to 30oC, its
heart rate will fall to 40-50 bpm. While this is
initially a protective response, if sustained, it can
lead to a decrease in respiratory rate, which may
in turn lead to cardiopulmonary failure. Also, a
hypothermic kitten will not suckle effectively, its
gastrointestinal motility will become depressed,
and it will have an increased susceptibility to
infection. It is therefore important to check the
temperature of any potentially weak or ill kittens.
However, if their rectal temperature is <34oC the
kitten is likely to die.
5. Inappropriate nutrition
Care should be taken to feed the queen an
appropriate diet. Incorrect nutrition of the
queen can affect the quality of the milk she
produces. Generally, when the queen is healthy
and producing adequate milk the kittens should
have no problems with inappropriate nutrition.
Inadequate milk production may be associated
with an inexperienced or overly nervous queen,
old queens, sick or malnourished queens,
dystocia, certain familial traits, systemic
illness or mastitis. Inadequate milk uptake by
the kitten can also result from anything causing
kitten ill-heath or weakness, from competition
and bullying by siblings, or any environmental
factor that distracts or upsets the queen-kitten
bond.
Normal kittens should suckle within 2 hours of
birth as they can only adsorb colostrum in the fi rst
16-24 hours of life. Since any kitten not gaining
suffi cient weight has an increased risk of neonatal
death it is important to weigh kittens regularly (at
birth, daily for the fi rst week, then at least twice
weekly until after weaning). A loss of <10%
may be expected in the fi rst 24h, but after that
there should be daily weight gain (~10-15g/day;
5-10%); they should double their birth weight
by 1-2 weeks of age and weight gain should be
steady and progressive. Any weight loss (or lack
of weight gain) should be investigated, and any
kittens losing more than 10% body weight are
unlikely to survive.
It is essential that kittens gain adequate nutrition
as they have a greater risk of developing
hypoglycaemia than adults. This is because they
are metabolically less able to generate glucose than
adults, while having a much larger requirement
for it. Any kitten that is ill or stressed may develop
hypoglycaemia. This may be seen as weakness,
hypothermia, crying, diffi cult breathing, seizures,
coma and, eventually, death.
Neonatal kittens are also very susceptible to
dehydration. This may result from inadequate
consumption of milk, or excessive fl uid losses
(usually associated with overheating, excessively
low humidity, or diarrhoea). Kittens contain
relatively more body water than adults and
their water turnover rate is twice that of adults.
Neonatal kitten maintenance fl uid requirements
are ~130-220ml/kg/24h, compared to 50-65ml/
kg/24h for a mature cat. This is because kittens
have greater fl uid losses through their skin, lungs
and kidneys, which are all immature.
Since the kittens derive all of their food and
water in the form of milk, when the supply is
inadequate, supplemental feeding is needed.
Where the kittens have been orphaned or the
queen is unable to feed them they will need
total replacement feeding (see FAB Manual).
Weaning should begin at 3-4 weeks of age.
It is important to ensure that all of the kittens
gain suffi cient food at this time. In large litters
competition at the food bowl can lead to weaker
kittens being bullied and so eat less.
6. Neonatal isoerythrolysis (NI)
In certain cat breeds NI is a relatively common
cause of fading kittens. It results from the immunemediated
destruction of a kitten’s erythrocytes by
its mother’s antibodies. The maternal antibodies
enter the kittens via the colostrum when the
kittens fi rst suckle. The kittens are born healthy.
However, after suckling, affected kittens may die
suddenly or stop feeding, become weak, and show
haemoglobinuria (brown stained urine). These
kittens may then develop jaundice, anaemia,
tachypnoea, and tachycardia. In severe cases this
leads to collapse and then death. Surviving kittens
may develop necrosis of the tail-tip and other
extremities, which may then slough between 3
days and 2 weeks of age.
Cats have 3 blood groups; Type A, B, and AB.
Type A is genetically dominant to Type B.
Genetically, a Type A cat may therefore be A/
A or A/b. The rare blood type AB is inherited
slightly differently, and is recessive to Type
A but dominant to Type B. AB cats are only
found in breeds in which the Type B has been
identifi ed, usually increasing in frequency as
the percentage of Type B cats increases. The
frequency of Type A, B and AB blood types
varies between breeds (Table below), and also,
to some extent, between countries. Generally,
most domestic short and longhaired cats (DSH/
DLH) are Type A (75-100% Type A; 0-25%
Type B; 0-10% Type AB). Interestingly, the
Bengal breed appears to have a particularly high
number of AB cats, although actual prevalence
data are not yet available.
All Type B cats have high levels of naturally
occurring antibody directed against Type A
erythrocytes, while only a third of Type A cats
have naturally occurring antibody directed
against Type B erythrocytes (and the amounts of
antibody are usually rather low). NI occurs when
a Type B queen gives birth to a Type A kitten.
When the kitten suckles colostrum the maternal
anti-A antibodies enter the kitten’s circulation
and attack its erythrocytes, causing anaemia and
jaundice. Since these antibodies occur naturally,
the queen does not need to be sensitised by
previous pregnancies or blood transfusions. Since
the highest proportion of Type B cats are seen in
BSH cats, NI is seen most frequently in this breed
of cat.
Where NI is seen, all sexually active cats should
be blood-typed to prevent further inappropriate
mating. In addition, it is recommended that
all BSH cats should be blood-typed prior to
breeding. This can be done using a simple inhouse
test card (Rapid Vet-H, dms laboratories).
It is important to ensure that Type B queens do
not mate with Type A toms. Where an unknown
mating has occurred, placental blood can be used
to determine a kitten’s blood type. If the queen’s
blood-type is known to be Type B, and a kitten is
found to be a Type A, it can be prevented from
suckling the queen, at least until it is >24h old.
While this procedure will prevent the occurrence
of NI, the lack of colostrum will leave the kitten
at risk of infectious disease.
Kittens showing signs of NI, if <24h old, should
be immediately removed from their mother to
prevent further absorption of anti-A antibodies.
In kittens, most colostral antibodies are absorbed
by 12-24h of age. Once removed, the kittens can
either be fostered to a Type-A queen, or fed milk
replaced formula for 24 hours. After this time it
is generally safe for them to be returned to their
dam. If the anaemia is severe a blood transfusion
will need to be performed (see separate notes).
However, despite removing the kittens as soon as
clinical signs are noted, most affected kittens that
die within their fi rst week of life.
7. Infection
In general, infections are involved in relatively
few early neonatal deaths. However, they can
result in signifi cant mortality from 3-4 weeks
of age onwards. Since neonatal kittens have
immature immune systems, and gain <5% of
their MDA transplacentally, they need to gain
protection from infectious disease via transfer of
MDA in the colostrum. The passive protection of
the intestines by MDA continues for the entire
duration of suckling as IgA antibodies resist gastric
degradation and can bind potential pathogens in
the gut lumen, preventing them from attaching to
or penetrating the intestinal mucosa. The ability
of neonates to absorb MDA begins to decline 6h
after birth, and is no longer possible after ~48h.
The majority of neonatal infections are caused
by agents to which vaccines are not available;
it is therefore important that neonates are born
into the same environment as their dam has been
living since she will then have raised antibodies
against its resident infectious organisms. The
protective effect of systemically absorbed MDA
usually begins to wane from 3-4 weeks of age.
The kittens’ natural immunity is still developing
at this time, and since most vaccine regimens do
not start until ~8 weeks of age, this can leave a
period of time when the kittens are particularly at
risk from these infectious diseases.
A healthy kitten should be able to cope with
a low level of infectious organisms within its
environment. It will generally experience no more
than occasional mild and brief clinical signs.
However, if the kitten’s immune system becomes
R
Table: Breed prevalence of feline blood types
100% Type A ~80% Type A 75-100% Type A 60% Type A 40% Type A
Siamese Somali DSH/DLH Devon Rex British Short
Hair (BSH)
Burmese Abyssinian Persian
Tonkinese Birman
Oriental Maine Coon
Norwegian Forest Cat
Cat
suppressed serious disease or fatal infections
may occur. Factors which may contribute to an
inadequate immune response include inadequate
colostrum intake, inadequate nutrition, low birth
weight, peri-natal hypoxia, congenital disorders
(especially of the immune system), previous trauma
or infection, a low environmental temperature, or
an unhygienic environment leading to a build up
of contamination with infectious agents.
Respiratory and gastrointestinal infections are
seen most frequently. (See FAB Manual, refs
and separate lecture for the treatment of sick
neonates).
Viruses
• The cat fl u viruses (feline calicivirus [FCV] and
feline herpes virus [FHV-1]) are perhaps the most
commonly seen viral infections of kittens. While
in healthy kittens infection may be mild and brief,
weak kittens may develop more severe clinical
signs or secondary bacterial infections. FHV-1
infection may also be associated with abortion.
• Feline coronavirus infection (FCoV), like
the cat fl u viruses, is hard to eliminate from
breeding catteries. When present infection may
be associated with an increased incidence of
reproduction failure, abortions and stillbirths.
Affected kittens may show signs of diarrhoea,
malaise, or ‘fading’, and occasional cases of more
classical effusive feline infectious peritonitis
(FIP).
• Feline panleukopenia virus (FPV) is usually
seen in catteries that fail to vaccinate properly.
It is occasionally seen in kittens from vaccinated
queens, possibly resulting from severe
environmental contamination. Infection may
result in abortions, stillbirths, fading kittens,
diarrhoea, panleukopenia, septicaemia, cerebellar
ataxia, and/or death.
• Feline leukaemia virus (FeLV) has been
almost eliminated from the pedigree breeding
population in many countries. Neonatal disease
caused by this infection is therefore seen mainly
in rescue catteries. In this situation it may result
in reproductive failure, abortions, stillbirths,
fading kittens, a panleukopenia-like syndrome,
septicaemia or death.
• (In puppies canine herpes virus is a common
cause of puppy loss, and can result in abortion,
or neonatal death associated with abdominal
distension and pain at <3weeks of age. Other
common viral infections of puppies include
canine distemper virus, canine parvovirus, canine
coronavirus [which appears to be changing
in signifi cance], canine adenovirus-2, and
parainfl uenza).
Where infectious disease is suspected it is
important to ensure that the queens’ vaccination
programme is up to date. Since kittens gain some
protection from infectious disease in the form of
MDA passed in the colostrum, it may help to give
booster vaccines prior to mating. In some cases
it may be appropriate to instigate an isolation
breeding and early weaning programme (see FAB
Manual).
Bacteria
In kittens, bacterial infections are often seen
secondary to viral infection (cat fl u, FeLV, FIV,
FPV, FIP). However, bacterial infections can
also be seen without prior viral infection. In most
cases the bacteria originate from the queen’s birth
canal (beta haemolytic Streptococcus sp. [Strep.
G infection]), gastrointestinal tract (E. coli,
Salmonella sp., Campylobacter sp., many normal
enteric bacteria), or respiratory tract (Bordetella
sp., Pasturella sp., Mycoplasma sp.). Clinical
signs depend on the site, nature, and severity of the
infection. They may include diarrhoea, coughing,
dyspnoea, polyarthritis, omphalophlebitis, or
dermatitis, as well as the less specifi c signs more
typical of fading kittens.
Ultimately, many of these infections may result
in septicaemia and death. The increased risk of
sepsis in neonates results from the factors listed
above, especially failure of passive transfer of
MDA. In addition, neonatal propensity to develop
hypoglycaemia and intestinal ileus (especially
when cold), signifi cantly increases the risk of
translocation of enteric bacteria into the blood
stream. This is exacerbated by sepsis further
predisposing to hypothermia and hypoglycaemia
(possibly resulting from impaired liver function,
depletion of glycogen, and peripheral utilisation
of glucose by bacteria and leucocytes). Disease
may be very sudden or may run a more protracted
course. While the clinical signs are varied, they
frequently result in bradycardia, dyspnoea,
dehydration, weakness, crying, seizures, coma
and death. Sepsis often occurs as the fi nal stage
of other conditions, and is particularly associated
with systemic viral infections. The most common
cause of sepsis are gram-negative bacteria, but can
include; Streptococcus, E. coli, Staphylococcus,
Klebsiella, Enterobacter, Enterococcus,
Pseudomonas, Clostridium, Bacteroides,
Fusobacterium, Pasteurella and Salmonella.
Parasites
In well-run catteries parasite infestation should
not be a problem. Where queens are not wormed,
heavy kitten infestations can result in a poor body
condition, soft or bloody stools, lack of appetite,
a pot-bellied appearance, weight loss, and
occasionally death. A severe fl ea, tick or hookworm
infestation can result in signifi cant anaemia. Gut
parasites, such as Giardia, Tritrichomonas foetus,
Isospora or Cryptosporidia may cause diarrhoea
and a failure to thrive. Toxoplasma infection may
result in abortion, stillbirths and fading kittens.

In general
Where specifi c infections keep recurring it may
be necessary to try to detect carrier animals.
However, since a number of infections can cross
between species, affecting both cats and dogs,
and even humans, it may be necessary to look for
carriers amongst pet dogs, or even the owners.
This is true for many of the bacterial and protozoal
gut infections (e.g. Salmonella, Campylobacter,
Giardia and Cryptosporidia), and can also occur
with Bordetella bronchiseptica (which is one of
the causes of ‘Kennel Cough’).
Table: Infectious agents which may cause disease in kittens
Respiratory tract Feline herpes virus (FHV) (Also called feline rhinotracheitis virus)
Feline calicivirus (FCV)
Chlamydophila felis (formerly Chlamydia psittaci)
Mycoplasma sp.
Bordetella bronchiseptica
Feline coronavirus (FCoV)
Gastrointestinal tract Feline panleukopenia virus (FPV)
FCoV
Salmonella sp.
Campylobacter sp.
Giardia sp.
Tritrichomonas foetus
Isospora sp.
Cryptosporidia sp.
Toxocara cati
Ancylostoma tubaeforme
Cutaneous Fleas
Lice
Otodectes sp.
Microsporum canis
Systemic Bacterial sepsis (Streptococcus sp., E. coli, Salmonella sp. etc.)
Feline leukaemia virus (FeLV)
Feline immunodefi ciency virus (FIV)
FCoV
FPV
Toxoplasma gondii
Misc. Staphylococcus and Streptococcus sp (bacterial omphalitis, polyarthritis)
General approach to unravelling causes of kitten
mortality
Trying to fi nd out what may be causing kittens
to ‘fade’ can be very diffi cult. Firstly, it is hard
to decide exactly when there is a signifi cant level
of neonatal mortality. Secondly, most cases are
multifactorial, so a number of factors may need to
be addressed in order to reduce mortality. Thirdly,
clinical signs are generally non-specifi c and the
small size of kittens makes collection of samples
diffi cult. Generally, concern should be raised
when pre-weaning losses exceed 20%, postweaning
losses exceed 10%, the number of losses
suddenly increases, or a particular cause of death
is seen more frequently than previously.
It is strongly advised that cattery owner’s should
keep detailed records of all animals within their
premises; including details of matings, litter
sizes and birth weights. All incidents of disease
should be noted. It is by noting changes in the
morbidity and mortality patterns that problems
can be recognised early. Using this data it may be
possible to track the spread of infectious disease
or determine the breed-line of a genetic disorder.
Since there are usually no particular clinical
signs that suggest a specifi c disease, investigation
usually involves looking at the entire cattery.
In most cases some aspect of the environment
is not ideal, or aspects of the management and/
or nutrition are unsound. A full investigation is
often needed before any recommendations can be
made. The investigator will need a background
history of the cattery and want to examine
all sick animals; looking for obvious signs of
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2006 World Congress WSAVA/FECAVA/CSAVA 720
trauma, congenital defects or disease. Because it
is diffi cult to collect blood samples from young
kittens the most useful samples are often collected
after a kitten has died. For this reason it can be
very useful to have post mortem examinations
performed on any kittens that die. The breeding
queens, particularly the mothers of any fading
kittens, should also be examined. Ideally, they
should be observed interacting with the rest of
the litter, then examined for signs of general ill
health, metritis, mastitis, or aggression towards
the kittens.
In order to determine if environmental factors are
involved, the investigator may need to visit the
cattery. They may want to look at the design and
construction of the premises, consider the source
of new stock, the genetic relationships between the
cats, the total number of cats (and other animals)
within the household, the size of any subgroups,
and the day-to-day cleaning protocols. They may
also want to discuss any recent changes in the
management of the cats (feeding, vaccination,
worming, fl ea treatment, use of isolation facilities,
etc).
It is useful to remember that a single design
defect or a particular bad practice rarely causes
an outbreak of disease. More typically, disease
outbreaks result from an ‘event cascade’, where
a number of different confounding factors come
into play.
(See separate lecture for specifi c treatment options
for sick neonates).


Useful references and information:
Blunden AS (1998) The Neonate: Congenital
Defects and Fading Puppies. BSAVA Manual
of Small Animal Reproduction & Periparturient
Care, p 143-152
Feline Advisory Bureau Manual of Cat Breeding
(2006), FAB Publications, Tisbury.
Feldman DC and Nelson RW (1987) Feline
reproduction. In: Canine and Feline Endocrinology
and Reproduction. Ed. Feldman DC and Nelson
RW, WB. Saunders, Philadelphia. pp. 525-548 (or
the 2004 edition).
Hoskins JD (1995) Fading puppy and kitten
syndrome. Kirk’s Current Veterinary Therapy XII,
eds. RW Kirk and JD Bonagura, WB. Saunders,
Philadelphia. pp. 30-33
Hotston Moore P and Sturgess CP (1998) Care of
Neonates and Young Animals. BSAVA Manual
of Small Animal Reproduction & Periparturient
Care, p 153-169
Little S (2004). Breed Specifi c Reproduction
Projects; Heritable Aspects of Cat Breeding;
Feline Reproduction: A Manual for Cat Breeders
and Veterinarians (CD ROM); www.catvet.
homestead.com , SusanLittleDVM@compuserve.
com
Sturgess CP (2006) Feline paediatric medicine.