Download Feline neonatal mortality

The Sick Kitten
Rachel Dean BVMS DSAM(fel) MRCVS, Recognised RCVS specialist in feline medicine
Associate professor in Feline Medicine, Director of the Centre of Evidence Based Veterinary Medicine,
School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington Campus. LE12
5RD
Tel: 0115 951 6575 Email: [email protected]
Kitten – young cat, sick – afflicted with ill health or disease, ailing
There are many conditions that can affect a kitten during the first 6 months of life. No
matter how small the kitten is a complete clinical examination and history is vital. If
the kitten is still with its litter mates or mother, then clinical examination of all ‘in
contacts is recommended.
These notes will focus on the first 3 months of life.
Feline neonates
Neonatal kittens that are presented to the veterinary surgeon during the pre-weaning
period provide a diagnostic challenge. In the absence of a major congenital defect,
clinical examination is often unrewarding. Abnormalities frequently detected in
neonates e.g. hypothermia are non-specific and therefore provide little information
about the underlying aetiology of the condition. Furthermore, by the time the breeder
has recognised a problem and brought the kitten to the surgery, he/she is already
critically ill.
As a consequence of the above, targeted treatment is often impossible and therefore
response to treatment is poor. This is further confounded by altered drug tolerance
and metabolism in young neonates, which limits the number of safe therapeutic
options available to the veterinary surgeon (see later).
It is important to remember that one ill neonatal kitten may reflect a greater problem
within a cattery. Establishing the extent and frequency of kitten losses to assess
whether it is acceptable is often warranted. The neonatal period, from birth to 34weeks of age, is critical. More kittens are lost during this period than any other time.
An acceptable kitten mortality rate is about 10% where approximately half of these
are stillbirths, however if the mortality rate is much higher then further investigations
are required. Post-mortem examination of any neonate can provide invaluable
information, particularly as neonatal kittens can show minimal clinical signs or die
unexpectedly.
The physiology and the main causes of death of neonatal kittens will be considered
but it is important to understand kitten development when approaching a
breeder/cattery/shelter with a high rate of pre-weaning kitten mortality.
Neonatal Thermoregulation
o
Kittens less than 3 weeks of age cannot regulate their own body temperature
and the shivering reflex does not start to develop until the kitten is at least one
week of age.
The range rectal temperatures of new born kittens are approximately:
Week 1: 35 - 37oC (95 - 99 oF)
Weeks 2 and 3: 36 - 38oC (97 - 100 oF)
Week 4: 38 - 39oC (100 - 102 oF)
o
Hypothermia is a major contributing factor to neonatal mortality and kittens’
body temperature will drop rapidly if separated from the queen. As soon as
body temperature starts to fall depression of the suckling reflex occurs and
the resultant hypoglycaemia is life threatening.
Neonatal Metabolism
o
The metabolic rate of neonates is 2 - 2.5 that of adult cats.
o
Neonates are very vulnerable to hypoglycaemia and regular suckling is
necessary to maintain normoglycaemia.
o
Hypoglycaemia is self-perpetuating as a decrease in blood glucose leads to
suppression of the suckling reflex exacerbating the hypoglycaemia and
hypothermia. At birth, kittens on average should weigh 100g, depending on
the breed (i.e. average Main Coon kitten weighs 120g, smaller oriental breed
kittens weigh 80g). Most kittens will lose weight during the first 24hours of life,
if this exceeds 10% bodyweight or if the weight loss continues for a longer
period then supplementary bottle-feeding should be instituted.
o
Young kittens should to sleep for 90% of the day – a very active noisy kitten is
an indication of problems in the litter.
Neonatal Haematology
o
Foetal red blood cells are still present until approximately 4 weeks of age.
They are larger than normal red blood cells (rbc) but there are fewer of them
so initially the PCV of a neonatal kitten is the same as an adult cat. However
the PCV of neonatal kittens decreases during the first 2-4 weeks of life. This
is a physiological anaemia due to the short lifespan of foetal rbc in circulation,
haemodilution due to expanding blood volume and a reduced rate of
erythropoeisis compared to an adult cat. The anaemia is not associated with
decreased oxygen carrying capacity as the concentration of 2,3diphosphoglycerate increases shifting the oxygen-haemoglobin curve to the
right. At 4 weeks of age foetal rbcs are replaced by neonatal rbcs and by 8
weeks of age a kitten will have a PCV similar to that of adult cats
o
The haemoglobin oxygen diffusion curve in neonates is shifted to the right,
compared to adult cats. This maximises the efficiency of oxygen transfer,
which coupled with their relative tolerance to hypoxia makes it worth
persisting with kittens that are reluctant to breathe following parturition.
Neonatal Nephrology
o
The glomerular filtration rate of kidneys in the neonate is approximately 1/3 –
¼ of that of an adult cat. This is due to a combination of smaller capillary beds
at the glomeruli, decreased permeability of the glomerular epithelium and/or
decreased systolic pressure. The concentration of neonatal urine is only 1.5
times the plasma osmolality. Hence kittens will drink more than an adult cat
and up to 200ml/kg can be normal for a neonate.
o
Neonatal kittens are therefore highly susceptible to dehydration.
Neonatal Immunology
o
In the neonatal period the immune system is poorly developed, with
decreased number of lymphocytes, no T-helper cell activity, no memory cell
production and reduced complement and neutrophil function.
o
Maternally derived immunity (MDI) is an important aspect of neonatal
resistance to infection. Negligible amounts of maternally derived antibodies
cross the placenta, so kittens are reliant on passive transfer via the milk.
Kittens can absorb antibodies up to 72 hours following parturition but the first
16 – 24 hours are considered the most vital. Regular booster vaccination of
queens, particularly just prior to mating, will help optimise MDI
The major causes of death in neonatal kittens can be split into 5 main categories:
1. Maternal factors
2. Management factors
3. Bacterial infections
4. Congenital disorders
5. Neonatal isoerythrolysis (NI)
1. Maternal Factors
From pregnancy through to weaning the queen plays a vital role in survival of the
neonate. Dystocia can be a significant factor in neonatal mortality. Particular attention
should be paid to the health of the queen, as she provides energy and warmth to the
underdeveloped neonates. The provision of MDI via colostrum is also the major
mode of protection against infectious diseases in the first few weeks. Paradoxically
the queen can act as a source infection either via the milk (mastitis), vagina or by the
introduction of umbilical infections (See bacterial infections below).
2. Management Factors
If a high neonatal death rate occurs during the first few days of life it is possible there
is a basic management problem and a visit to the cattery should be considered. As
hypothermia and hypoglycaemia are major causes of neonatal death (see above),
environmental and management factors should be investigated. Environmental
temperature, humidity, hygiene and privacy for the queen should all be considered.
Kittens need to suckle regularly and rely on the queen for warmth. If the environment
is inappropriate the queen/kittens will spend time moving rather than feeding/sleeping
predisposing the kittens to hypoglycaemia and hypothermia. Nutrition of the queen is
important to avoid obesity during pregnancy, which has been associated with
increased rates of dystocia, and to ensure adequate production of milk and minimise
weight loss during lactation.
3. Bacterial infections
Infection is a relatively unusual cause of neonatal death. However bacterial
septicaemia can occur and the most important route of infection is via result umbilical
cord (omphalophlebitis). This infection may be from the vaginal during parturition,
from the queen’s saliva or from the environment. Omphalophlebitis can rapidly
extend to hepatic abscessation, peritonitis and septicaemia through haematogenous
spread via the umbilical vein. A kitten with bacterial septicaemia will deteriorate
rapidly with minimal clinical signs, and often several within a litter will be affected. If
infection is suspected and the causal agent is unclear, a broad-spectrum antibiotic
with efficacy against gram-positive and gram-negative organisms is advised.
Neonatal Pharmacology
Neonatal kittens have different susceptibilities to the toxic effects of some
regularly used drugs. This is due to different enzyme systems, altered renal
function, reduced plasma protein levels and increased permeability of the bloodbrain barrier, which can influence blood and tissue loads. They also have a large
surface area:weight ratio, so any drug which impairs thermoregulation is
hazardous. Foetal haemoglobin is also more susceptible to oxidation as levels of
methaemoglobin reductase are reduced, so oxidant drugs such as
sulphonomides and phenothiazines should be used with caution.
Antibiotics:
If there is suspicion of sepsis in a neonatal kitten, ampicillin, penicillins and
cephalosporins are considered relatively safe.
Tetracyclines, sulphonamides, aminoglycosides, and chloramphenicol are
considered unsafe due to toxic side effects and impaired secretion.
N.B. Viral infections are more likely to affect kittens during the post-weaning period
as MDI wanes prior to vaccination (see later).
4. Congenital disorders
Many body systems can be affected by congenital disorders, some are clinically
obvious physical defects and others e.g. metabolic defects, will go unnoticed. The
abnormalities can arise from genetic disorders or from teratogenic drugs (e.g.
griseofulvin). If the defect is severe then it may result in neonatal death, however
other cats can live a normal life with quite severe abnormalities e.g. pericardialperitoneal hernia. A congenital defect should be suspected in any kitten that is failing
to thrive or has a reduced growth rate
A note on Flat-chested kittens (FCK) and Pectus excavatum (PE)
These conditions are the most common congenital chest wall abnormalities, and both
defects can potentially reduce thoracic volume and compress the heart and lungs.
FCK becomes apparent during the first few weeks of life, and is seen as an
angulation of the ribs at the costachondral junction making the ventral part of the
thoracic cavity flat. Mildly affected cats will be asymptomatic; moderate to severely
affected kittens will have poor weight gain and exhibit difficulty breathing. Severely
affected individuals die as neonates. PE is an upward displacement of the sternum
towards the thoracic spine. If the defect is severe dyspnoea, weight loss or failure to
thrive may become apparent. A less severely affected kitten may have reduced
growth rates but can survive to adulthood. With both conditions if the kitten survives,
the defect will become less pronounced as the cat matures.
5. Neonatal isoerythrolysis (NI)
Cats have 2 major blood groups – type A and types B. Type A cats have low levels of
naturally occurring antibodies against type B rbc, but type B cats often have
significant levels of naturally occurring antibodies against type A rbc. Blood type A is
dominant to blood type B. NI occurs when a type B queen is mated with a type A
tom, which will result in some (dependant on whether the tom in homogenous or
heterogeneous type A) type A kittens. The kittens are born healthy however once
they start to suckle maternally derived antibodies are transferred via colostrum.
These antibodies rapidly led to the destruction of foetal rbcs and within 2 - 3 days of
parturition kittens will stop feeding and become weak, jaundiced, have
haemoglobinuria, or die suddenly.
NI can be avoided by blood-typing both queen and tom prior to mating, and avoid
mating type A toms with type B queens. Rapid vet H blood typing cards (DMS
laboratories) have made the determination of a cat’s blood type readily available to
veterinarians. Certain pedigree breeds e.g. British shorthair and Devon rex, have a
much higher prevalence of type B cats so blood typing these cats prior to breeding is
advisable. An alternative strategy is to identify the type A kittens by using drops of
blood from the umbilical cord. The kittens should then be removed from the queen for
the first 16-24 hours and receive colostrum from another queen.
The ‘older’ kitten
The disease seen in the kittens if they progress beyond the neonatal period are often
due to infectious pathogens. This is due to:

Waning (or lack of) maternally derived antibodies

Increased exposure to potential pathogens due to increased activity, outdoor
access, rehoming etc

Management factors similar to those for neonatal cats
It is possible that other congenital defects such as portosystemic shunts, peritoneopericaridal hernia, metabolic and cardiac defects may be noted at this age but often
these conditions remain silent until later in life. The nutrition of cats at this age is very
important. The diet must be of good quality, be a complete diet and be the correct
kitten formulation. It is essential to provide adequate nutrition throughout the weaning
period to ensure there are enough nutrients for growth.
Whatever the clinical problem kittens of this age are extremely vulnerable and can
deteriorate rapidly if their clinical signs go unnoticed. These notes will give a brief
overview of the pathogens which may affect kittens from 6 – 12 weeks of age.
The majority of pathogens which affect kittens of this age will either lead to
gastrointestinal signs, predominantly vomiting, and respiratory tract signs. The
exception is feline infectious peritonitis, due to feline coronavirus which is most
situations causes transient diarrhoea. This pathogen will be covered in other notes.
Common pathogens that may lead to gastrointestinal clinical signs include:

Isospora and Cryptosporidium spp
Infection with these two pathogens is often asymptomatic and is most commonly
encountered where there are high numbers of cats. Severe diarrhoea and weightloss
is sometimes seen in compromised individuals; hence underlying disease should be
looked for if infection persists. Often with adequate nutrition (sometimes a
prescription highly digestible diet is helpful) the kitten will respond without treatment.
Effective antibiotic treatment for kittens with these infections is problematic.
Remember that Cryptosporidia has zoonotic potential

Bacteria spp e.g. Campylobacter spp, Salmonella spp, Clostridium difficile and E.
Coli
Bacterial causes of diarrhoea are probably less common than viral or protozoal
infections, but infection with certain pathogens can have serious consequences.
Avian strains of Salmonella typhimurium have been recently reported to cause
diarrhoea and in some cases mortality in cats in the UK. The cases occurred
between September and February and the syndrome has been termed ‘songbird
fever’. A positive culture can also be found in asymptomatic acts, so faecal cultures
should always be interpreted with caution

Tritrichomonas foetus
This pathogen is relatively ‘new’ to feline medicine and can cause severe large
intestinal diarrhoea. It is often seen in young cats but they are mostly over 12w of
This pathogen can be distinguished from Giardia on a fresh faecal smear due to its
‘jerky forward’ movements as it is propelled by the three flagellae that give this
pathogen it’s name. There are now PCRs available to diagnose this pathogen and
the author often does this if the clinical signs are suspicious of T. foetus and a faecal
swab is negative. The current treatment of choice is Ronidazole (similar to
Metronidazole which has no activity against T foetus) which can be difficult to source
and then dose accurately and reversible neurotoxicity has been reported following
overdosing of cats. Cats with T foetus infection can have diarrhoea for months.

Giardia spp
Infection in young kittens often leads to an acute diarrhoea. Infection is most
common in cats kept in large groups. A recent study of faecal samples from 250
(adult) cats in the USA showed a prevalence of Giardia of 13.6% using faecal
flotation and immunoflourescence. This is much higher than previous studies. Also
75% of the cats shedding Giardia spp were also shedding Cryptosporidium oocysts
(Vasilopulos et al). Giardia can be difficult to diagnose on faecal examination. It is
worth collecting at least 3 consecutive faecal samples from a cat that you are
suspicious may have Giardia. Giardia has a ‘falling leaf’ motility which differentiates it
from T. foetus.
Helminths
Toxocara cati and Toxascaris leonina are the most common helminth infections that
cause diarrhoea in cats and are readily eliminated by routine anthelmintics.

Feline panleukopenia virus (FPV)
FPV is now rarely seen in countries where routine vaccination in commonplace.
However if vaccination is not available clinical signs are seen and can be
devastating. Sudden death is a common presentation, though some cats will have
peracute diarrhoea. A cat with severe diarrhoea and a marked lymphopenia, should
be treated as an FPV unless proved otherwise. Once FPV is in a household or
shelter the effects can be devastating.

Feline coronavirus (FCoV)
Most kittens will have antibodies to FCoV as this is a highly contagious pathogen
that is common in open cat populations and normally causes mild transient
diarrhoea. A positive antibody titre DOES NOT indicate a cat has feline infectious
peritonitis (FIP) – a rare consequence of FCoV infection.
Common pathogens that lead to upper respiratory tract infections in young kittens
include:

Feline herpesvirus (FHV)

Feline Calicivirus (FCV)

Chlamydophila felis (C felis)

Bordetalla bronchiseptica

Mycoplasma spp
All of these infections will give none specific clinical signs and without further
diagnostics it is not possible to be certain which is causing disease. FHV, FCV and
C. felis are most commonly encountered, and a kitten is often infected with more than
one pathogen at once. Disease is often seen in vaccinated cats as the vaccines do
not create a sterilising immunity and if the viral load is high the immune system can
be overcome.
Tips for diagnosing and treating these infections include:

FHV causes ocular lesions as well as respiratory signs, most commonly
dendritic corneal ulcers

FCV causes lingual ulceration as well as respiratory signs

Skin lesions are also seen occasionally with FHV infection

C felis is purely an ocular pathogen than only affects the conjunctiva and will
not cause corneal ulceration.

Polymerase Chain Reactions are reliable for the diagnosis of FHV and
C.felis, but are more problematic when diagnosing FCV, so virus isolation is
recommended for diagnosing this pathogen

Supportive and symptomatic treatment is paramount for kittens with FHV and
FCV. Anti-viral treatment has limited success.

Kittens with C felis should be treated with systemic antibiotics, 10mg/kg SID
Doxycyline for 4 weeks is the treatment of choice. Clavulonate-potentiated
amoxicillin can be used as an alternative if there is concern of enamel
discoloration.
The role of Bordetella and Mycoplasma in respiratory tract disease is often debated
as there is little evidence in the literature about these infections. Upper and lower
respiratory tract signs can be observed with these infections and the infections can
be lethal