Environmental toxins can cause fading puppy and kitten syndrome. Bedding materials and products used to clean the whelping
or queening box should be evaluated for safety in neonates. Neonatal skin is thin, and chemicals can be more readily absorbed
transcutaneously in a neonate than in an adult.11 Respiratory tract exposure to chemicals can also be a concern. Avoid pine oils and phenols as well as direct contact with
bleach or quaternary ammonium residue.12 Use gentle cleaners with little odor, and remove all residue before contact with the neonates.
GENETIC AND CONGENITAL FACTORS
Detailed pedigree analysis, including the coefficient of inbreeding (COI), can often lend insight into the cause of neonatal
losses. Deleterious homozygous genes can result not only in decreased litter size because of early embryonic loss but also
in increased neonatal mortality. In research colonies of purebred dogs, litters with a low COI (0 to 0.25) had a 10-day mortality
rate of 26.5%.13 Highly inbred litters, with a COI of 0.734 to 0.785, had a 10-day mortality rate of 73%.13 Breeding of siblings or continued line breeding results in increased mortality rates when the COI is greater than 0.375.13 Pedigree software programs to determine the COI are readily available with databases for a variety of breeds.*
Gross abnormalities can be found in many ill or deceased neonates. Cleft palates and lips, atresia ani, portosystemic shunts,
open fontanelles, and cardiovascular abnormalities are relatively common. In one study, 20% of kittens that were stillborn
or died within three days of birth had gross anatomical abnormalities.4 Inborn errors of metabolism are likely even more common but are difficult to diagnose. Swimmer (flat) puppies and kittens
can be identified by dorsoventral flattening and lateral widening of the thorax. The cause is unknown but probably relates
to both genetic and environmental factors. Pectus excavatum is a more severe deformity resulting from intrusion of the sternum
into the thoracic cavity.
Thymic dysfunction and atrophy can result in a fatal wasting syndrome in neonates.14 The critical period for this appears to be 3 to 6 weeks of age, as experimental removal of the thymus during this time is
fatal.14 Thymic atrophy can result from stress, corticosteroid administration, toxins, malnutrition, viral diseases, and zinc deficiency.14 Evaluating the thymus is an important part of necropsy in any deceased neonate.
Low birth weight is an important risk factor for neonatal mortality.1,15,16 Kittens have a normal birth weight of 100 ± 10 g (3.5 ± 0.35 oz). Kittens with a birth weight of less than 90 g (3.2 oz)
have poor survival rates.15 In one study, 59% of kittens that were stillborn or had early neonatal deaths had low birth weights.1
While puppy birth weight varies with breed, there are estimates for a variety of breed sizes. Pomeranian birth weights average
120 g (4.2 oz), beagles 250 g (8.8 oz), greyhounds 490 g (17.3 oz), and Great Danes 625 g (22 oz).17 Average birth weights may vary within breeds according to family lines; breeders often have records helpful for comparison
Pups and kittens may lose a small amount of weight (< 10%) during the first 24 hours of life, but after that, weight gain
should be steady. Pups should gain 5% to 10% of their birth weight daily, while kittens should gain 7 to 10 g (0.25 to 0.35
oz) a day.18,19 Failure to gain is a clear early sign of potential problems in a neonate and should be addressed immediately.
Transient juvenile hypoglycemia syndrome is associated with low weight, particularly in toy-breed dogs.7 Because of limited glycogen stores, poor gluconeogenesis, and high metabolic rates, failure to maintain frequent feedings
can result in hypoglycemia. This can occur for several weeks to months in toy breeds and often arises when the pups are transferred
to a new home where feeding schedules are not rigidly followed.20